Professional Documents
Culture Documents
Q Banks Points PDF
Q Banks Points PDF
Q Banks Points PDF
Kaplan:
Prosopagnosia: inability to recognize faces. Usually caused by
bilateral lesion of visual association cortex.
Anosagnosia: deficit in recognition about one's illness, due to
lesions of the non-dominant parietal lobe.
UW:
The benefit from smoking cessation is the single most important
modifier of mortality.
Mortality modifiers include:
Aspirin therapy and tight blood glucose control.
Diet
Phenylalanine
BH4
Phenylalanine hydroxylase
Defected in PKU
Tyrosine
Tyrosine hydroxylase
Tetrahydrobiopterin
( BH4)
Alpha methyl
Dopa ( dihydroxyphenaylalanine )
tyrosine inhibits
PLP
This cofactor is also required by:
Phenylalanine hydroxylase
NO synthase
Tryptophan hydroxylase, which is used
to make serotonin and melatonin. Those
three in addition to tyrosine
hydroxylase. Defect in dihydrobipterin
reductase ( responsible for making
tetrahydrobipterin ) also results in
PKU
This enzyme is
induced by cortisol.
Dopa carboxylase
Dopamine
Vit C
this enzyme.
Used only in
pheo.
Nore-epi.
Phenylethanolamine-Nmethyltransferase ( PNMT ).
SAM is required here because
this is a methylation step.
COMT and MAO are the enzymes responsible for brake down of
catecholamine.
Epi
Nore epi
COMT
MAO
Dihydromandalic acid
Noremetanephrine
COMT
Metanephrine
MAO
Vanillylmandelic
acid ( VMA )
Tyrosine metabolism: UW
Dihydrobiopterin reductase
BH4
Phenylalanine
PKU:
Autosomal recessive
Mental and growth retardation
Seizures, fair skin, eczema
Mousy oder
Tyrosine become essential
Usually due to phenylalanine hydroxylase deficiency.
Small % due to BH2 reductase deficiency ( this is
known as malignant or atypical PUK ).
Melanin
( in melanocytes )
BH2
Phenylalanine
hydroxylase
Tyrosine
DOPA
Homogentistic acid
( alkapton )
Homogentisate oxidase
Catecholamine
Maleylalacetoacetate
Alkaptonuria:
Autosomal recessive
Dark connective tissues ( homogenstic
acid binds to collagen ).
Fumarylacetoacetate
Pigmented sclera
Urine turn black on standing due to
oxidation of homogentistic acid.
Debilitating arthralgias
Fumarate
TCA cycle
Excess accumulation of
phenylalanine or its products
leads to brain damage in PUK.
Phenylalanine
Phenylacetate
Phenylpyruvate
Phenyllacetate
Tryptophan
BH4
5-hydroxytryptamine
Serotonin
B6
Niacin
NAD/NADH
Melatonin
Steroid receptor
bound to HSP
Nucleus
Hormone-receptor complex
Steroid
Methemoglobinemia, UW:
Fe+++
Methemoglobin
Neimann-Pick
Choline
Ceramide
Glucose
Sphingomyelin
Krabbe's
Gaucher
Glucocerebroside
Glactocerebroside
Metachromatic
leukodystrophy
Fabry's
Ceramide trihexose
Galactose
Gangliosides (GM3)
Tay-Sachs
Sulfatides
e.g. Cerebroside
sulfate
Gangliosides (GM2)
Sphingolipids break down occurs in the lysosomes and just takes the reverse
pathway. When one of the breakdown enzymes is deficient, lysosomal storage disease
results ( 6 are sphingolipidosis, and 2 are mucopolysacharidosis, Hurler and Hunter ).
The above diagram shows only sphingolipidosis.
> Pick and GaUcher have Big ( hUge liver ). Pick has red macula, Gaucher is not.
> Pick and Tay-Sac have red maculae. Pick has Big liver, Sac is not.
> Hurler is blind, Hunter is not.
Ceramide
Krabbe's
Sphingomyelinase
Gaucher
Beta Glucocerbrosidase Beta galactocerbrosidase
Sphingomyelin
Glucocerebroside
Metachromatic
leukodystrophy
Arylsulfatase A
Fabry's
Alpha galactosidase A
Ceramide trihexose
Galactocerebroside
Gangliosides (GM3)
Hexosaminidase
Tay-Sachs
Gangliosides (GM2)
Nemonic:
Upper raw : NGK ( No Guy Killed )
Lower raw : FTM ( For That Money )
Sulfatides
e.g. Cerebroside
sulfate
Angiokeratoma of Fabry's
Hepatosplenomegally,
Cherry-red macula and
foam cell of Niemann-Pick
Tay-Sacks
No hepatosplenomegally ( VS Niemann )
Whirled
Brain problems
Niemann-Pick
Zebra bodies
Big organs
Hepatosplenomegally
Huge organs
Gausher's
No red macula ( VS Niemann )
Crunched up paper
Aseptic bone necrosis
All of them cause severe neurological deterioration except Gaucher, which spares the
brain and affects the liver.
Fabry's
Metachromatic
leukodytrophy
Angiokertomas
Ataxia
Hurler's
Gargoylism
Hunter's
Corneal clouding
Associated
Variable
Trastuzumab
Breast cancer
RET
Experimental
NEN 2a and 2b
PDGF-R
Imatinib
c-KIT
Imatinib
ABL
Imatinib
Variable
Internet:
Warm antibodies are IgG in nature and are formed against Rh antigen (D antigen) and
these can cross the placenta. this antibody is responsible for Hydrops fetalis in Rh
incompatibility. Also IgG antibodies produced in Auto Immune Hemolytic anemia where IgG
antibody coated erythrocytes are destroyed in the spleen.
Cold antibodies are IgM in nature and are produced against ABO blood group, responsible
for hemolysis in ABO mismatch transfusion. Also IgM antibodies are produced in certain
infections like Mycoplasma pneumoniae called Cold Agglutinins which can causes
hemolysis. In case of cold antibodies -the IgM binds to RBC and Activates complement and
it is complement mediated hemolysis and this occurs intravascularly.
Cord factor
Cord factor refers to trehalose dimycolate, a virulence factor
and glycolipid cell-wall component of virulent strains of
Mycobacterium tuberculosis and closely related species. It is a
surface glycolipid which blocks macrophage activation by IFN-,
induces secretion of TNF and causes Mycobacterium
tuberculosis to form cords in vitro. This is the main virulence
factor for the mycobacterium tuberculosis that makes it
resistance to anti-tuberculosis medications.
Mycobacterium that does not have this cord factor is not able
to cause disease.
H. Influnzae
T.B meningitis
Cryptococcus : pigeons
Histoplasma: bats, birds, caves
Path. UW:
Neuroblastoma is the most common extracranial childhood cancer.
Develops from neuroblast located in the adrenal medulla.
2 yrs old
Solid sheets of small cells with dark nuclei and scant cytoplasm
Renal mass, HTN, anorexia
Associated with N-myc amplification
FA:
The most common tumor of the adrenal medulla in children. Can
occur anywhere along the sympathetic chain. Homovanillic acid
(HVA), a breakdown product of dopamine, elevated in
urine. Less likely to develop hypertension. Overexpression of Nmyc oncogene associated with
rapid tumor progression.
P
SH proteins,
SOS proteins
SH proteins,
SOS proteins
Inactive
MAPkinase
Gene transcription
Active
Ras-GDP
Ras-GTP
Inactive
Active
Pi
MAPkinase kinase
RAF
RAS-MAP kinase
PI3K/Akt/mTORA
Inositol phospholipid
cAMP
JAK/STAT
Prolactinomas, UW:
Cystic fibrosis, UW
In milder forms of CF where increase in sweat chloride is not seen we can perform this
transepithelial difference. there is less chloride secretion but relatively increased Na and water
absorption, hence increased negativity on the membrane ie incresed potential difference.
Cl
CFTR
Cl
Secretion
Sweat
UW, cardio:
The best auscultatory indictor for mitral stenosis severity is
the length of interval between A2 and the opening snap. They
are inversely related, i.e. The more severe the stenosis is, the
shorter the interval between A2 and OS. In modren practice
however, the severity of MS is determined by measuring the
transvalavular pressure gradient using 2D doppler.
While the best auscultatory indictor for mitral regur. severity
is S3 gallop of the left ventricle.
Early adenoma
Small adenoma
K-Ras
Late adenoma
Large
P53, DCC
Adenocarcinoma
APC : is a tumor suppressor gene. It controls cellular division, intercellular
attachment, and cellular movement ( with the tissue and out of the tissue ).
K-Ras: a protooncogene. Mutated K-Ras encodes for a protein that has no
ability to inhabits cell cycle but stimulate it ( growth signaling system ).
Note: aspirin aspirin impedes progression from adenoma to carcinoma.
Colonic polyps
Adenomatous (70%)
Can develop into cancer
Divided into tubular and villous
Nonadenomatous (30%)
Very low risk
Hyperplastic and other
less common types
Translocations:
8:14
The resultant
Increased c-MYC
11:14
Increased Cyclin D
14:18
Increased BCL2
9:22
Ph+
The tumors
Burkitts
Follicular lymphoma
CML
Desmosomes/ HemiDesmosomes:
HemiDesmosomes, the
linking protein is
integrin.
Basal lamina
BCL2
Apoptosis
BAX
Failure of repair
In the event that there is excessive DNA damage, the BAX gene is
activated. BAX gene inhibits the BCL2- antiapoptosis gene causing release
of cytochrome C from the mitochondria and apoptosis of the cell.
Type I
Accounting for approximately 20% of RPGN, type I RPGN is characterized by the presence
of autoantibodies directed against the glomerular basement membrane (GBM). It is also
called anti-GBM glomerulonephritis. The antibodies are directed against a particular protein
found in the GBM, type IV collagen, specifically the noncollagenous region of its 3 chain.
In addition to the anti-GBM antibodies, some cases of type I RPGN are also associated with
antibodies directed against the basement membrane of lung alveoli, producing Goodpasture
syndrome. The majority of type I disease, however, features anti-GBM antibodies alone;
these cases are considered idiopathic.
Type II
RPGN caused by the deposition of immune complexes accounts for 25% of RPGN and is
classified as type II. Thus any immune complex disease that involves the glomerulus may
progress to RPGN if severe enough. These diseases include systemic lupus erythematosus,
acute proliferative glomerulonephritis, Henoch-Schnlein purpura, and IgA nephropathy. While
polyarteritis nodosa also involves vasculitis associated immune complex deposition that can
lead to renal failure, it is not considered part of type-II RPGN because it mainly affects
medium sized vessels and does not necessarily involve the kidneys.
Type III
Also known as pauci-immune RPGN, type III RPGN accounts for 55% of RPGN and features
neither immune complex deposition nor anti-GBM antibodies. Instead, the glomeruli are
damaged in an undefined manner, perhaps through the activation of neutrophils in response
to anti-neutrophil cytoplasmic antibodies (ANCA). Type III RPGN may be isolated to the
glomerulus (primary, or idiopathic) or associated with a systemic disease (secondary). In most
cases of the latter, the systemic disease is an ANCA-associated vasculitis such as Wegener
granulomatosis, microscopic polyangiitis, or Churg-Strauss syndrome.
Classification of type III RPGN into primary or secondary may be unnecessary, as primary
type III RPGN and secondary type III RPGN may represent a spectrum of the same disease
process.
The ANCA form may have a more favorable response to treatment than other forms.
Type IV
Type 4 has features of both types 1 and 3. This is also called "double-antibody" positive
disease.
Hemeangiomas: UW:
Strawberry hemangioma ( infantile ) is the most common
benign vascular tumor in children. May regress spontaneously.
Cherry hemangioma most common benign vascular tumor in
adult.
Apoferritin
Iron
Ferritin micelle
Hemosiderin
methylmalonyl-CoA
Succinyl CoA
Neurotoxic
CH3
B12
Active
Folic acid
CH3
Inactive
B12
Inactive
Folic acid
Active
Metabolic acidosis
Increased anion gap:
MUD PILES
M- methanol
U- uremia
D- DKA
P- paraldehyde or phenformin
I- iron tablets or INH
L- lactic acidosis
E- ethylene glycol
S- salicylates
Sepsis
Shock
Hypoxia
Garage
House
Lactam ring
Its the garage that is always affected.
Bacterial genetics
Four ways by which bacteria can exchange genetic material:
1. Transformation
2. Transduction
3. Conjugation
4. Tranposon
# Transformation: one bacteria lysis, the others take pieces of its genome.
# Transduction: via bacteriophages. Two types of phages:
1. Virulent: invade the bacteria, replicate, kill the bacteria and pop out. As it does so, some
of the bacterial genetic material might get into one of these new phages and get
transduced into another bacteria.
2. Temperate phage: invade the bacteria, incorporate its DNA into the bacterial DNA and
wait as a prophage ( of course its DNA will be replicated with the bacterial DNA ). The
infected bacteria is termed lysogenic ( because it may lyse at any moment should the
repressor protein is damaged, for e.g. by UV light ). And the virus is called lysogenic
phage. Eventually, the prophage will be activated ( If the repressor protein, that prevent
the synthesis of virus specific proteins, is mutated ), the bacteria lyses and the phage is
released to infect another cell ( said to enter the lytic cycle or become lytic phage ).
The term lysogenic immunity is used describe the ability of the prophage ( the hidden
virus ) to prevent another phage form entering its cell.
Transduction has two types:
1. Generalized: virulent phages are involved in this
2. Specialized: temperate phages are involved in this. This occurs because the temperate
virus inserts itself only in predetermined area in the bacterial DNA. e.g. The lambda phage
of E. coli that inserts itself between the genes that are responsible for biotin and
galactose. If the cell turned into lytic cycle, one of these genes ( not both ) might get
packaged with one of the new phages and get into a new cell. The bacteria that get this
new gene would said to undergo lysogenic conversion ( see next page ).
Note: phage repressor is made by the bacteria to prevent the virus from producing its
structural protein. If the bacteria fail to produce this repressor, the virus will rapidly
produce the proteins that is in need of, assembles and lyse the cells ( lytic cycle instead
of lysogeinc cycle )
Intermediate filaments
Mutated in progeria
Sensory Corpuscles
1. Pacinian: P for Pressure. Its for pressure and vibration, they
are deep seated in the joints and ligaments.
2. Meissner; as the way you say it, it's smoother that Merkle, so
meissner is for soft(light touch). Found on hairless (soft) skin
areas, palm sole, nipple, and tongue.
3. Merkle's; hard texture as the way you say it, so it's for harsh
touch or harsh edges, found at hard skin areas(hairy).
4. Anything else is free nerve ending and it's for pain and
temperature.
Collagen
Strong
Elastin
Stretchy
Proline, glycine
Glycosylated
Nonglycosylated
Degerated by elastase
alpha antitrypsin inhibits
elastase.
Neurotransmitter
NE
Location of synthesis
Locus ceruleus, reticular formation
and solitary tract
Preoptic is not a
"true" hypothermic.
It belongs
developmentally to
Preoptic nuclei
telencephalon but
Optic tract
Optic chiasm
functionally to
diencephalon. It
regulates the
parasympathetic NS.
Anterior -4
Middle -3
Posterior -2
Above downward:
Above downward:
Above downward:
1. Paraventricular: oxytocin
1. Dorsomedial nucleus: stimulates
1. Posterior
2. Anterior hypothalamic: cause the GIT results in obesity ( no as
hypothalamic:
body cooling ( AC ). Controls
important as ventromedial ).
cause body heating
the parasympathetic. Releases 2. Ventromedial nucleus: satiety
( PH ). Control
GnRH.
center ( feeding center is located
sympathetic NS.
3. Suprachiasmatic: circadian
in an area known as lateral
2. Mammillary
rhythm. See next page ...
hypothalamic zone ).
body: limbic
4. Supraoptic: ADH
3. Arcuate nucleus: regulates the
system.
ant. pit.
If you zap your lateral nucleus, you shrink laterally.
If you zap your ventromedial nucleus, you grow ventrally and medially.
Ventromedial
Lateral
Anterior
Posterior
Arcute
Paraventricular
Supraotic
Suprachiasmatic
Retina
Dark
Suprachiasmatic
NE release
Melatonin
Sleep
Pineal
Pharyngeal arches:
1st arch:
Arch of Ms and Ts
Innervated by mandibular
and maxillary branches of
ptrygoids , myohyoid ).
2nd arch:
Arch of Ss
CN VII (facial
expression)
smile
3rd arch:
The word pharyngeal
SHSH
Don't give beta blocker to patients with cocaine induced HTN, that would
worsen the BP.
Beta blockers are the DOC in patients with aortic dissection.
Cytokines
Hot
Bone stEAk
IL-1 fever
IL-2 stimulate T cells
IL-3 stimulate bone marrow
IL-4 IgE and IgG
IL-5 IgA and eosinophils
IL-6 an acute phase reactant, comes from macrophages ( like IL-1)
INF Alpha: an acute phase reactant, comes from macrophages.
Mediates septic shock.
IL-8: from macrophage. Major chemotactic factor ( the I in the
nemonic click.
IL-10: induces Th-2 and inhibits Th-1
IL-12: induces the differentiation of T cells into T helper 1 cells.
Activates macrophages
INF gamma: activates macrophages
Bone marrow
Class effect
Rito
Indi-, Ataza-
Class effect
Efavirenz
Efavirenz causes neuropsychiatric effects. Its teratogenic.
NRTIs
Protease inh.
NNRTIs
Zidoviudine
Zidovudine
Zidovudine
Zidu + lami
Protease inh.
HAART
Pharmacokinetics Equations
MC
The 4 equations:
1. Vd= amount of given drug [IV]/
plasma concentration
2. Clearance= 0.7*Vd/T half
3. LD= Css*Vd
4. MD= Css*Clearance
T half= 0.7*Vd/ clearance
Given: clearance = 2L/hr
Vd= 0.5 L/kg*60 = 30 L
So T half = 0.7*30/2 = 10.5
LD= Css*Vd
LD= 20 mg/L * 30 L = 600 mg.
This 10 mg/L is the half of the previous target dose. So we have to wait
for one half to pass.
MD= Css* Cl
= 10 mg/L* 2L/hr
= 20 mg/hr
MD= Css* Cl
LD= Css* Vd
Obviously, only MD is affected by clearance. It should be
decreased.
Non fermentor
Oxidase test
Fermentation speed
Positive
Negative
Fast fermentors
P. arginosa
Slow fermentors
E. coli
Klebsiella
Enterobactor
Serratia
Citrobacter
TSI Test
H2S
No H2S
Shigella
Proteus
Salmonella
Physiologic intervention
Respiration
Valsalva
Standing
Squatting
Passive leg raising
Handgrip
GnRH
LH
FSH
Testosterone
Inhibits beta
subunit of LH and
that of GnRH
Semenepherous tubule
containing Sertoli cell
Laydig
Basal Ganglia
Antipsychotics (neuropleptics)
High potency - "Try to Fly High"
Trifluoperazine, Fluphenazine, Haloperidol
(extrapyramidal signs)
Low potency - "Cheating Thieves"
Chlorpromazine, Thioridazine
(non-neurologic SEs: anticholinergic, antihistamine, alpha blockade)
dsDNA fracture
Pyrimidine-pyrimidine Ultraviolet
dimers
Homologues or non
homologues religation
Ultraviolet specific endonuclease
that causes nick at the damaged
site that are later excised by the
5'-3' exconuclease activity of DNA
polymerase.
Deamination
Spontaneously or
chemical
Streptococci
Alpha hemolytic
Beta hemolytic
Optochin
Bacitracin
Sensitive
Resistant
S. pneumina
Viridans
Ps are sensitive
Gamma hemolytic
Sensitive
Resistant
S. pyogen
Agalactiae
Grow in bile
AND 6.5 NaCl
Enetrococci ( E. feacium )
Class 1 antiarrythmia
Virion
CMV
EBV
HIV
Rabies
Rhinovirus
Cellular receptor
Cellular integrins
CR2 ( CD 21 )
N and M receptors
ICAM1 ( CD56 )
Nucleotides:
Cidofovir
Tenofovir
Activated nucleotides
polymerase
> Cause chain
termination.
Viral Genetics
Reassortment: two segmented viruses. These are Arena, Bunya, Orthomyxo ( like
the ABO system ) and Reo. ( 2,3,11,8 segments respectively ).
Recombination:
Occurs in non-fragmented viruses. There would be an exchange in genomic
material between two chromosome via crossing over within homologous region .
Transformation: generally defined as the uptake of naked DNA by a prokaryotic or
eukaryotic cell. In virology, used to describe the incorporation of viral DNA into a
host cell chromosome.
Phenotypic mixing: just the nucleocapsid acquisition. No genomic exchange so no
new cytopathic features.
Interfering: one virus inhibits the replication and/or the release of the other
virus. No genomic exchange.
Blotting Technique
DNA
RNA
Proteins
Secretory
Cell membrane
Etc
Metabolites
Folate antagonist
Methotrexate
Purine analogues
Pyrimidine analogues
5-flurauracil
Cytarabine and
other 'abine'
members.
Pathophysiology Of SIADH
Excessive ADH secretion
Water retention
Transient, SUBCLINICAL,
extracellular volume expansion
Decreased aldosterone and
increased ANF.
Dilutional hyponatremia
Further Na loss
Euvolemic hyponatremia
Normalization
of extracellular
fluid volume.
Glucose Transporters
Characteristics feature
GLUT1
RBCs, CNS
GLUT2
Liver, Pancreas
GLUT3
GLUT4
GLUT5
Sperms, GIT
Fructose transport
Hemangiomas
These are two types: Capillary and cavernous hemangiomas
Capillary hemangiomas are :
Strawberry hemangioma
Cherry hemangioma
Nevus flammeus ( aka port-wine stain )
Pyogenic granuloma
# Strawberry hemangioma ( infantile, juvenile, premature ):
Appear since birth
Regress spontaneously
Bright red when in the epidermis, when deeper they are more violaceous.
# Cherry hemangioma ( senile )
Benign capillary hemangioma of the elderly.
Does not regress.
Frequency increases with age
Cutaneous and not found in mucosa and deep tissues
# Nevus flammeus ( aka port-wine stain ):
Mature capillaries.
Sharply demarcated, irregular, flat patch that commmonly involves
the face.
Associated with Sturge-Weber disease
Fleshed colored ones regress, discolored ones persist
# Cavernous:
Dilated vascular spaces with thin-walled endothelial cells
Blue, large compressible masses
Less likely to regress
Associated with VHL
Could occur in the mucosa or deep tissues.
Associated nerve
Trigeminal
Facial
Glossophayrngeal
PA
AA
Superior laryngeal
( vagus )
Obliterated
Recurrent laryngeal
( vagus )
carotid
True aortic arch and subclavian
artery
Obliterated
Pulmonary artery and ductus
arteriosus.
Purkinje System
Atrial Muscle
Ventricular Muscle
Slowest
AV Node
Lipid Lowering
High LDL
Hypertriglyceridemia
Low HDL
Still low
Still high
Still high
Statin
Still high
Ezitamibe
Fibrates
Still high
Niacin
Niacin
Minus
Absolute risk
Treatment
Absolute risk
Control
NNH = 1/ ARI
NNT = 1/ ARR
ARI = Event rate of treatment - event rate of control
ARR ( AR ) = Event rate of control - event rate of treatment
INH:
Rifampin
Ethambutol
Pyrazinamide
Streptomycin
Bacterial Toxins
# Both shiga toxin and cholera toxin are encoded by bacterial
chromosomes (Chromosomal Encoded Somethings = Cholera,
Endotoxin, Shiga toxin )
# Phage coded toxins pnemonic is OBED:
O Ag of salmonella
Botulinum toxin
Erythrogenic toxin of S. pyogens
Diphtheria toxin
Shiga-like toxin
# Other toxins and Multiple drug resistance -- Plasmid
Skull openings:
Skull openings:
Cribriform plate
Olfactory
Optic canal
Optic nerve
Oculomotor
Trochlear
Trigeminal - Ophthalmic
Abducens
Foramen Rotundum
RoMax
Trigeminal - Maxillary
Foramen Ovale
OMan
Trigeminal - Mandibular
Facial
Vestibulocochlear
Jugular Foramen
Glossopharyngeal
Vagus
Accessory
Hypoglossal
Hypoglossal Canal
63
68
70
71
71
72
72
77
80
82
82
90
Staph. epidermitis
Strept. sangus and mutants
Viridant group
Pseudomonas
Nontypable H. influenzae
Edward
Patau
AFP
Normal
B-hCG
Normal
Estriole
Inhibin
Normal
Normal
Normal
Thalamus
VPL
Cortex:
BM area
1,2,3
VPM
Visual sensations: LGB
Auditory sensations: MGB
So, all sensations relay in
the cortex except smelling.
Dopamine Agonists
Ergot Componds
Bromocriptine
Pergolide
Non-ergot Compounds
Pramipexole
Ropinerole
Double stranded
UvrB
Nick
UvrC
Deamination
Xanthine
Hypoxanthine
Uracil
3'
5'
Deoxyribose AP site
3'
5'
DNA polymerase fills the gap and a ligase seals the nick.
Mismatch repair system ...
4. The gap is then filed with DNA polymerase delta and the nick is
sealed with ligase.
5'
1. Ataxia Telangectasia:
2. XP:
DNA is hypersensitive to UV
3. Fanconi anemia:
4. Bloom Syndrome:
5. HNPCC:
Atheroma Formation
Intimal injury ( say by HTN or DM ) leads to expression of vWF by
endothelial cells. vWF traps platelets leading to platelets plug
formation and WBC recruitment.
Also LDLs might get beneath the basement membrane of the tunica
intima worsening the inflammation that has begun with platelet.
Continued LDL deposition leads to fatty streak formation.
Macrophages engulf the LDL and become foam cells.
Injured endothelium release growth factors that promotes smooth
muscle cells ( SMC ) migration and proliferation such as PDGF. These
SMC are responsible for intimal thickening by producing collagen,
elastin and proteoglycans.
Work of Breathing
Minute ventilation= tidal volume*RR
When the elasticity of the lung is increased most of work is done during
inhalation. And the larger the tidal volume the patient takes, the 'bigger'
the work he is going to exert. As such, patients with restrictive lung
diseases tends to decrease the tidal volume. And to maintain the same
minute ventilation, the tends to increase the RR.
In obstructive diseases, most of the work is done during expiration. And
as the patient increases his RR, more and more work is exerted. As such,
these patients tend to decrease the RR and increase the tidal volume
( to maintain the same minute ventilation ).
Work of breathing
The least work
RR
15
Normal
10
Obstructive:
Slow, deep.
20
Restrictive:
Rapid, shallow
Antihistamines
First generation:
Anti-H1, anti-M, anti-serotonergic and alpha adrenergic. They are
lipophilic and as such, the could cross the BBB.
You must first chant "dimen, diphen, chlorphen" before you fall
asleep: dimenhydrinate, diphenhydramine, chlorpheniramine. These
are more sedating.
Added to these are promethazine and meclizine.
Second generation: devoid of anti-M, anti-serotonergic and alpha
adrenergic properties. They cant cross the BBB and are less
sedating: Don't Let u Fall aSleep
Desloratadine, loratadine, fexofenadine, cetirizine.
Sarcomere Anatomy
Zoe Is A Horny Mama!
Effects Of Glucocorticoids
Liver:
Increase proteins
synthesis, esp. those of
gluconeogenesis and
glycogen synthesis .
Peripherally, they
antagonize the effect of
insulin leading to
increased catabolism of
adipose and muscular
tissues.
Bone:
Decrease bone density by
Inhibiting GI Ca absorption
Increase renal Ca excretion.
Inhibit bone forming
activity of osteoblast.
Immune system:
Decrease lymphocyte count
especially CD4.
Decrease eosinophils
Increase neutrophils
Skin:
Inhibits fibroblast
proliferation and collagen
formation leading to
thinning of the skin.
Esophagitis
Endoscopic findings
Candida
Herpes
CMV
Microscopic finding
Patches of grey/white
pseudomembranes on
erythematous background.
Eosinophilic intranuclear
inclusions ( Cowdry type
A ) in multinuclear giant
cells at the margin of
the ulcer.
Linear
ulcerations
Torsade
Benzos
BZ 1 receptor - for SEDATION therefore Sleep disorders = Temazepam &
Oxazepam. (Mnemonic I use is "go TO sleep")
BZ 2 receptor - for anxiolysis therefore Anxiety disorders = Lorazepam,
Diazepam, Midazolam and Alprazolam.
Diazepam is the longest acting (24 to 36 hours).
Midazolam is shortest acting (4 hours, therefore its used in pre-op induction
anesthesia)
Oxazepam, Temazepam & Lorazepam are metabolized Outside The Liver. (OTL)
Also, they increase the frequency of opening of Cl- channels as compared to
Barbiturates which increase the duration.
HBV
P53 inactivation
Cellular proliferation
Other mutations as
a result of chronic
inflammation.
In PCOS, LH is increased increasing androgens and FSH is decreased with resultant build
up of androgen leading to many of the features of the syndrome, e.g. Hirsutism.
LH
Progesterone
Androgens
Cholestrol
Theca interna
Androgen synthesis
Testosterone
FSH
Granulosa
Estrogen
Estradiol
Contain aromatase
Granulosa
Theca externa
( fibrous capsule )
Theca interna
Alzheimer
Late
Assocaited with epsilon 4
allele of Epolipoprotein E4.
Drugs ( Nitrites )
Fe2+
( e.g. in Hb )
Fe3+
( MetHb )
NH4
Astrocyte
Accumulate and
cause damage
Glutamine DH
Glutamine
Glutaminase
Glutamate
Glutamine
Glutamine
synthase
Alpha KG
TCA
Glutamate
NH4
NMDA
AMPA
Hyper NH4 affects the brain in two ways: 1. Neuron are affected because excess
ammonia favor the formation of glutamate depleting the cell from alpha KG, an
important substrate for TCA. 2. Glutamine built within the astrocytes a toxic
levels.
Fen-phen
Fenfluramie and phentermine are appetite suppressant drugs
that causes pulmonary hypertension and cardiac valvular
problems.
Vitamin D
7-dehydrocholesterol
( Provitamin D3 )
UV light ( 290-350 )
Previtamin D3
Isomerization induced by heat
Cholecalciferol
D2 ( Plant derived )
( Vitamin D3 )
25-hydroxycholecalciferol
1,25 dihydroycholecalciferol
1 alpha hydroxylase in the
kidney.
24,24 dihydroycholecalciferol
Biologically inactive made when
there is 1,25
dihydroycholecalciferol excess.
PTH
Proopiommelanocortin
POMC a polypeptide!
beta-Endorphins
ACTH
MSH
Polyol Pathway
Glucose
Aldose
reductase
NADPH
Glycolysis
NADP
Sorbitol
Sorbitol
dehydrogenase
NAD
NADH
Fructose
Active factor X
Inactive factor X
Unfractionated heparin
PLUS
Antithrombin
Thrombin
Inactive thrombin
Active factor X
LMWH
Plus
Inactive factor X
Antithrombin
LMWH only inactivate because due to its short length, that
renders it unable to bind to thrombin.
GnRH
Hypothalamus
GnRH agonists:
Leuprolide
Goserelin
Nafarelin
LH
Ant. Pit
Testosterone
Ketoconazole
Leydig cell
Cholesterol
Spironolactone
DHT
Peripheral tissue
Androgen-receptor
complex in target cell
Desomlase
Pregnenolone
Finasteride
Flutamide
Cyproterone
Nuclear receptors
Thyroid hormones
Retinoids
Perioxisomal proliferating activated receptors
Fatty acids
Kallikrein
Kininogen
Plasminogen
Plasmin
Bradykinin
ACE
inhibitors
ACE
Inactive
products
Fibrin
C1 C1 esterase
Activated C1
C1 esterase inhibitor
Angioedema
Time line
0-4 hr
4-12 hrs
12-24 hrs
1-5 days
5-10 days
10-14 days
2 wks to 2
months
MI
Minimal changes
Early coagulation necrosis,
edema, hemorrhage and wavy
fibers.
CVA
Coagulation necrosis
Auto-antibodies
Hurtnup Vs Fanconi
In hurtnup, there is aminoacidouria restricted to neutral amino acids.
This urinary excretion of proline, hydroxyproline and araginine remains
unchanged. This in contrast to Fanconi, in which there is generalized
aminoacidouria.
-ve selection
Subcaspular zone
Positive for all of TCR,
CD3, CD4, and CD8
( double positive )
Cortex
Aptosis
Positive
Medulla for CD4,
CD3 and
TCR
No excessive affinity
Survival
Excessive affinity
for MHC
Aptosis
No excessive affinity
Survival
Minors Consents
CPS-2
Carbomyl-P
Deficiency leads to
oratic aciduria
Oratic acid
White crystals appear in urine
Hydroxyurea
UMP
Ribonucleotide
reductase
dUMP
CH3
Thymidylate
Synthestase
dTMP
5FU
5-deoxyuridine
CMP
NH2
dCMP
Ribonucleotide
reductase
Hydroxyurea
Bacterial vaginosis
( MCC of vaginitis )
Signs and Sx
Thin, off-white
discharge with
fishy odor.
No inflammation
Candida
Vluvovaginits
Trichomoniasis
( 2nd MCC of vaginitis )
Malodorous, graygreen, thin, frothy
vaginal discharge
Inflammation
Laboratory test/
microscopy
PH> 4.5
Clue cell
Positive whiff test
( amine odor with
addition of KOH )
PH> 4.5
Motile trichonads
First line Rx
Mitronidazole
Mitronidazole or
tinadazole
Must Rx sexual
partner
2nd line Rx
Clindamycin
None
Thick, white
discharge that
adherent to vaginal
wall.
Inflamed
Normal PH
( 3.8-4.2 )
Pseudohyphae
Fluconazole
Polythysemia Vera
EPO receptor
EPO
Janus kinase -2
STAT
Translocate to nucleus,
control proliferation of
myeloprogintor cell
Mutated Janus
Kinase -2,
phosphorylated
without EPO.
Sleep apnea
PTH receptor
Vitamin D receptor
Osteoblast
RNAK ligand
Osteoprotegerin
Osteoprotegerin is a protein
secreted from mesenchymal cells
and acts as a decoy receptor,
decreasing the interaction
between the RANK L and its
receptor, inhibiting monocytes
maturation into osteoclasts.
Monocyte colony
stimulating factor
( MCSF )
Monocyte
MCSF and RANK L
stimulate monocytes to
mature into osteoclast.
Calcitonin receptor, the
only receptor on
osteoclasts. It inhibits
osteoclasts.
Osteoclast
The ratio between RANK L: OPG determines bone turn over. Higher ratio leads to bone
resorption. RANK receptors are over expressed in hypoestrogenic states, accelerating
bone turn over.
A decoy receptor, or sink receptor, is a receptor that binds a ligand, inhibiting it from
binding to its normal receptor. Etanercept is another example of a decoy receptor.
See next page for VitD
Vit. D receotor
Vit. D
Osteoblast
Alkaline phosphatase
Alkaline phosphatase makes the appropriate
solubility product to mineralize cartilage and
bone.
Beta stimulation
increase insulin
secretion.
Alpha stimulation
inhibits insulin
secretion.
Beta cell
Insulin
Beta brings!
Nuclear Receptors
1-Retinoid receptor (Vit A)
2-Calcitriol receptor (Vit D3)
3-T4/T3 (T3 binds more avidly)
4-Fatty Acids bind to PPAR
5-PPAR -alpha (Fibrates)
6-PPAR -gamma(Thiozolidinedions)
Cytoplasmic receptors
1. Androgen
2. Estrogen
3. Progestins
4-Glucocorticoids (e.g Cortisol)
5-Mineralcorticoids (e.g Aldosterone)
Leucine
Neurotoxicity
Isoleucine
Valine
Deformation
Disruption
Sequence
Agensis
Ulcer Vs Erosion
Ulcer
Erosion
Mucosa
Musclaris mucosa
Submucosa
Muscularis propria
Serosa
Axonal reaction
Neuronal atrophy
Type of injury
Transient severe insult that
lead to cell death
Loss of axons
Progressive degenerative
disease
Histologic change
Shrinkage of the cell body
Pyknosis
Loss of Nissl substance
Eosinophilic cytoplasm
Loss of neurons
Reactive gliosis
Xanthomas
Typically associated with hyperlipidemia and
lymphoproliferative malignacies
1. Eruptive Xanthomas: hypertriglycerides
2. Tuberous and 3. Tendinous Xanthomas
4. Plane Xanthomas: in skin folds. Associated with PBC
5. Xanthelasma: no associated lipid abnormality in 50% of the
affected individual.
Vancomycin
Blocks glycopeptide
polymerization by binding
tightly to D-alanyl-D-alanine
Linezolid
Thrombocytopenia
Optic neuritis
High risk for
serotonin syndrome.
Apolipoprotein Functions
1. ApoLP to Functions:
A-I Activates lCAT (LCAT) (I look like non-cap L)
C-II Cofactor for lipoprotein lipase
E rEmnant uptake by Liver. Without these, liver cant clear remnants.
B Both main TG trasporter start with ApoLP B on their membrane:
- Chylomicron (secreted from intestine) have B48. Mediates chylomicron assembly
and secretion by intestine.
- VLDL (secreted from liver) have B100. Mediated LDL uptake by extrahepatic
tissue.
(The Intestine have to process food 1st in order to have material for Liver.)
The chains of processing is:
Chylomicron > Chylomicron remnant
VLDL > IDL > LDL
HDL
2. Both main transporters of Triglyceride (TG) to tissue (1 from Intestine
Chylomicron, and 1 from Liver VLDL) carry 3 ApoLP: B (B48/chylomicron, B100/
VLDL), C-II and E.
3. After they gave TG to tissue (C-II and LP Lipase role), they loss C-II, then
only B and E left on Chylomicron remnant and IDL.
4. After return the remnant to liver, they loss E, then only B left on LDL.
5. HDL role is to take Cholesterol back to liver: so it has A-I (to Activate LCAT to
make Cholesterol Ester), and E (to go back to liver afterward).
Result:
Chylomicron (B48,C-II,E) > Chylomicron remnant (B48,E)
VLDL (B100,C-II,E) > IDL (B100,E) > LDL (B100)
HDL (A-I,E)
DNA polymerases
Prokaryotic Polymerase
# All DNA polymerases [ I, II, III ] have proofreading activity to remove
mismatched nucleotides via 3'5' exonuclease activity.
# Only DNA polymerase I has 5'3' exonuclease activity to remove and
replace RNA primers.
# DNA polymerase III is responsible for DNA synthesis in the leading
and lagging strands
Eukaryotic polymerases:
: primase, but also adds a few DNA to the newly-made primer.
: repair.
: mitochondrial polymerase.
: lagging strand. Protein PCNA attaches to it with the help of RFC.
Proofreads.
: leading strand. Proofreads.
Colon cancers
HNPCC- associated colon
adenocarcinoma
Sporadic colon
adenocarcinoma
Age of occurrence
Younger than 50
Older than 50
Location
Predominately left
sided
Multiple cancers
Uncommon
Source
Adenomatous
polyp
Genetic bases
Adenoma
carcinoma
sequence
Hemoglobin Electrophoresis
Anode ( attracts
anions )
ANP
Kidney
Afferent arteriole
dilatation
Smooth
muscles of the
blood vessels
Adrenal gland
Decrease aldosterone
Vasodilation and
extravasation
Increased GFR
Increased urinary
excretion of Na and H2O
Syphilis
Tertiary:
Many years after infection
Primary:
Chancre
Secondary:
Desquamating rash
on palms and soles.
Condylomata lata
in untreated individuals.
1. Neurosyphilis:
Asymptomatic
Subacute meningioencephalitis
Tabes dorsalis
Others
2. CVS:
Ascending aortic aneurism
and resultant aortic
regurgitation.
3. Gumma:
Initially painless but when
ulcerate they become
painful.
Usually cutaneous but could
occur sub.Q, liver, bones,
and others.
Collagen, again!
Procollagen
Procollagen peptidases
Deficient in E-D
Tropocollagen
Aggregation
Collagen
Out side of
fibroblasts and
SMCs
Osler nodes: Oslers nodes (painful, palpable, erythematous lesions most often
involving the pads of the fingers and toes). Caused by immune complexes (they want
you to know that for Step 2). Infectious endocarditis and Roth spots are also due to
immune complexes leading immune vasculitis.
Janeway lesions (nontender, macular lesions most commonly involving the palms and
soles). Janeway lesions occur more frequently in endocarditis caused by
Staphylococcus aureus. Janeway lesions are caused by septic emboli. Subcutaneous
abscesses are found on histologic examination.
Splinter hemorrhages aka fingernail hemorrhage: narrow, red to reddish-brown lines
of blood beneath the nails. They run in the direction of nail growth and are named
splinter hemorrhages because they look like a splinter beneath the fingernail. The
hemorrhages may be caused by tiny clots that damage the small capillaries under
the nails or by vessel damage from swelling of the blood vessels (vasculitis). The most
common cause for splinter hemorrhages is trauma to the nail.
Weber Test
Neurosensory:
Softer sound
Conductive:
Louder sound
Rinne test
Chromosomal Translocations
Burkitt's Lymphoma : 8urkitt's Lymphoma = t(8:14). CMYC
Mantle cell lymphoma : mantle ce11 lymphoma = t(11:14). Cyclin D
Follicular lymphoma ( 18 letter ) = t(14:18). Bcl-2
Others:
CML: Ph. Chromosome = t(9:22). Abl
Acute promyelocytic leukemia = t(15:17)
ALL = (12:21). Associated with good prognosis
Seizure
Generalized
Partial
Carbamezapine
Absence
Euthoaximde
Valproic
Myclonic
Tonic-Clonic
Phenytoin
Carba.
Valproic
Valporic
Ca
Ca
Alcohol
Vicious pancreatic
secretion ( alcohol
induces high protein
content )
Spasm of
sphincter of
Oddi
Hemicholinium
Choline
Choline
AcCoA
Bromoacetylcholine
Acetylcholine
Ca
Ca
Choline
Acetate
Acetylcholine
esterase inhibitors
Botolinium
Atropine
Scala vestibuli
Oval window
Stapes
Round window
Scala tympani
Basilar membrane
Helicotrema
Acute Hepatitis
1%
Fulminant hepatitis
95%
Complete resolution
50-80%
Stable chronic hepatitis
4-5%
Chronic hepatitis
20-50%
Cirrhosis
10%
HCC
Blotting Technique
Substance detected
Northern
RNA
Southern
DNA
Western
Protein
Southwestern
DNA-binding protein
Type of probe
Single stranded DNA or
RNA ( hyberidization )
Antibody
Double stranded DNA
Renal Calculi
Ca oxalate or
Ca phosphate
70-80%
Radioopaque
Struvite ( Mg
ammonium
sulphate or
triple
phosphate )
15%
Radioopaque
5%
Radiolucent
Cystine
1%
Radioopaque
Ca oxalate or
Ca phosphate
Struvite ( Mg
ammonium
sulphate or
triple
phosphate
Uric acid
Cystine
Neuropeptide Y
Neurons
POMC
Neurons
Wight gain
Neuropeptide Y
Neurons
POMC
Neurons
Wight loss
Congenital QT prolongation
Metabolic acidosis
Bicarb loss
Acetoacetyl-CoA
HMG-CoA reductase
Fibrates
7-alpha hydroxylase
Estrogen
Cholesterol
Bile acids
Bile
Gall bladder
Gibbs free energy describes the both the direction in which a chemical
reaction will tend to proceed and and the concentration of reactants and
products that will be present at equilibrium. It can be calculated by the
following equation:
Deta G = - RTInK
Eq
Retroperitoneal organs
Vessels: aorta, IVC and their branches
Solid organs: pancreas except the tail, kidneys and suprarenals
Holo organs: part 2,3 of the duodenum and part of part 4, the
ascending and descending colon, rectum, ureters and bladder.
Vertebral column and pelvic organs
NPH
Neither paroxysmal nor nocturnal
GPI protein
This proteins anchors CD55 and CD59 proteins to
RBCs surfaces. These CD proteins inactivate complex
preventing hemolysis and thrombosis.
Normal
NPH
Empysema
Tobacco stuff
Proteinase 3
Cathepsin G
Elastase
Matrix metaloprotinase
Proteases
Antioxidants
Free radicals that inhibit
antiprotease activity of alpha 1
antitrypsin.
Oxidants
Samter's Triad
Asthma, aspirin hypersensitivity and nasal polyposis. Occurs in
10% of patients with asthma treated with aspirin. The polyps
develop due to high concentrations of leukotrienes that results
from the fact that aspirin inhibits COXs pathways shunting all
arachidonic acid products to lipooxigenase pathway.
TTP: Adults
HUS: pediatrics
Renal failure
CNS manifestations
Glucagon ( liver )
Epinephrine ( muscle )
Increased cAMP
Glycogen break
down.
Cognitive disorders
2
Coefficient of determination = ( the correlation Coefficient )
Likelihood ratio =
Sensitivity
1specificity
Types Of Studies
Descriptive Studies
Individual level
Case report
Case series
Cross-Sectional
Population level
Correlational ( ecologic )
Analytic Studies
Observational Studies
Case-Control
Cohort
Interventional
Randomized clinical trial
Ubiquitin
Mallory bodies, Lewy bodies, and neurofib tangles are all examples of
ubiquintation.
Oxaloacetate
Malate
NAD
Pyruvate
NADPH
G-3-P
DHAP
NADH
FAs synthesis
TG backbone
NAD
Pyruvate
NADH
Lactic acidosis
NAD
Acetoacetate
NADH
NAD
Acidosis
Homocysteinuria
Def: excess homocysteine in urine. Caused by three genetic defects ( lucus
heterogeneity ):
1. Cystathionine synthase deficiency
2. Decreased affinity for cystathionine for B6
3. Homocysteine methyltransferase deficiency
Homocysteine
Methionine
methyltransferase
B12/folate
Cystathionine
synthase
Homocysteine
B6
Cystathionine
Cysteine
Cluster Designations
CD
CD1: histiocytes
CD3: all T cell
CD4: Helper T cells
CD8: Cytotoxic T cells
CD10: this is the marker for most common leukemia in children; B
cell leukemia. It known as CALLA and that is common ALL antigen.
CD15, 30: RS cell
CD21: B lymphocytes
CD45: every WBC
Osmolarity Vs Osmolality
Both of them is defined as the concentration of osmotically active
particle in a solution. The difference is this:
In Osmolarity, this concentration is expressed in terms of osmoles
of solute per kg of the solvent.
While in Osmolality, this concentration is expressed in terms of
osmoles of solute per litter of the solution.
Osmole: the amount of substance that dissociate to form one
mole of osmotically active particle. E.g. One mole of glucose =
one osmole because its not ionizable. But one mole of NaCl = 2
osmoles because it dissociate into Na and Cl, all of which is
osmotically active.
Anyhow, Dr. Goljan says that the difference between these two is
garbage!
PAO2
PaO2
Cellular O2
Measured by ABG
Low O2 here =
hypoxia
1. High altitude:
# In high altitudes, P. Atm drops while other parameters, e.g. fiO2, stays the
same, i.e. 0.21.
# This will lead to low PAO2 and subsequently low PaO2.
# As such, no A-a gradient
# When the patients is given high conc. O2, e.g. 100%, his/her PaO2 rises.
# In these high altitudes, hypoxemia leads to hyperventilation which clear
more PCO2, giving more room for O2. Remember, in the equation, PCO2 is
subtracted.
Hyperventilation will lead to resp. alkalosis which is corrected after days by
the renal system via bicarb excretion. And by the way, this is the only acid
base disturbance in which the body is able to fully compensate for it.
2. Hypoventilation:
( P. Atm - H2O vapor pressure )* 0.21 - PCO2/0.8 = 150 MMHg
# The major consequence of hypoventilation is increased PCO2
in the alveoli which forces alveolar O2 to go down as will. This
will result in low PaO2, i.e. hypoxemia.
# This means there is no increase in A-a gradient ( see the
equation for A-a gradient below:
- PaO2
a
= 16
3. Diffusion
# Gas diffusion from alveoli to capillary is impaired.
# This could either be caused by interstitial deposits that prevents
O2 from diffusing, or because RBCs has been speed up so no enough
time for O2 to get to them as might occur in exercise.
# This would lead to increased A-a gradient.
# It does respond to supplemental O2.
4. Shunting
Alveoli
Pulmonary
artery
50%
70% sat
Examples of shunts:
Revered ASD, VSD, PDA
ARDS ( many alveoli are taken out
by the fluid in them ) and
pulmonary edema ( same as ARDS )
5. V/Q mismatch
20%
98%
P.E
89%
70%
80%
80%
# V/Q mismatch is the MCC of hypoxemia because the causes for this are so
common: pneumonia, pulmonary embolism ( see the PE diagram above ), COPD.
# There is increased A-a gradient
# It respond to O2
A-a gradient
High A-a gradient
PaCO2
High
Hypoventilation
Responds to supplemented O2
Low
High
altitudes
Yes
V/Q mismatch
Diffusion limited
Clinically differentiated
No
Right to
left shunt
Arms
Legs
Descending
ArmsAscending
Eosinophilia
Note:
Protozoa, e.g. Malaria parasite, do not induce eosinophilia. Only
INVASIVE helminthes do.
Cytotropoblast
Synctiotropoblsat
Wharton jelly
Blood sinusoid
Blood vessel
O2
Macula densa,
detects low Na.
Afferent arteriole
Metabolic Acidosis
All in here!
Metabolic acidosis is caused by low CHO3. CHO3 because low via one of
two ways:
1. Gain of H+ ions
Increased anion gap
Metabolic alkalosis
Saline resistant
Saline sensitive
Urine Cl > 20 Eq/L
Urine Cl < 10 Eq/L
Causes:
Causes:
1. Vomiting
2. Diuretics
1. Hyperaldosteronism
2. Patter syndrome
Pathophysiology:
Pathophysiology:
Rx:
Saline resistant: treatment of the
cause, e.g. Surgical resection of the
This would be called hypokalemic,
tumor.
hypochloremic metabolic alkalosis.
Volume contraction contribute much to the Saline sensitive:
Normal saline + potassium.
pathophys.
Hypersensitivity Pneumonitidis
Hypersensitivity pneumonitis (farmers lung, silofillers dz, bysinosis)
These are restrictive lung dzs.
Dont confuse farmers lung and silofillers dz they are BOTH seen in farmers.
So, remember one, the other is the other!
Silofillers dz put things in silos, which is a closed space, and fermentation of
gas occurs, the gas is nitrogen dioxide
Example: farmer went into a room in his barn and suddenly developed
wheezing and dyspnea, why? B/c he took in nitrogen dioxide, which is a
fermenting problem. (silo can explode b/c gas from fermentation).
Farmers lung thermophilic actinomyces (a mold).
Example: on tractor, dust being blown up in the air and thermophilic
actinomyces(which is a mold) is inhaled; leading to hypersensitivity and HPY
pneumonitis and they end up with a restrictive lung dz.
Bysinosis worker in textile industry(Lenin,cotton ,hemp), and they get
dyspnea.
Workers feel better over the weekend (no exposure to antigens), depression
occurs when returning to work on Monday .
These are the HPY and restrictive lung dzs.
Eosinophilia
Eosinophilia is the state of having high eosinophil granulocytes in the blood.
Normal ranges are between 0 and 0.5 109 per litre of blood. Eosinophilia is
presence of more than 450 cells/microL in blood.
The release of interleukin-5 by T cells, mast cells and macrophages
stimulates the production of eosinophils.
Diseases that feature eosinophilia: They can be easily be remembered by
the famous mnemonic "CHINA".
C - Connective tissue diseases
H - Helminthic (ie, worm) infections
I - Idiopathic HES
N - Neoplasia
A - Allergies
Connective tissue disease
# Eosinophilia-myalgia syndrome (due to tryptophan in the United States
in 1989)
# Rheumatoid arthritis
# Toxic-oil syndrome (due to contaminated rapeseed oil in Spain in 1981)
# Churg-Strauss vasculitis
# Coccidioidomycosis fungal infection
# Eosinophilic fasciitis
Parasitic infestations
# Ascariasis
# Schistosomiasis
# Trichinosis
# Strongyloidiasis
# Visceral larva migrans
# Gnathostomiasis
# Fascioliasis
# Paragonimiasis
Idiopathic hypereosinophilic syndrome
Neoplasia
# Lymphoma (e.g. Hodgkin lymphoma, non-Hodgkin lymphoma)
# Adult T-cell leukemia/lymphoma (ATLL)
# Human T-cell lymphotropic virus I (HTLV-I)
# Gastric or lung carcinoma (i.e. paraneoplastic eosinophilia)
# Eosinophilic leukemia (very rare)
Allergic
# Asthma
# Allergic rhinitis
1. B-cell: A, B, C
A: selective Ig A Deficiency
B: B ruton's
C: C ommon variable immunodeficiency
2. T-cell: TICH
T: Thymic aplasia
I: IL-12 deficiency
C: chronic mucocutanous candidiasis
H: hyper-IgE syndrome ( Job's ). Don't confuse it with hyper IgM
syndrome.
3. Combined B and T cell deficiencies:
SCID
Ataxia Telangectasia
Hyper-IgM syndrome
Wiskott-Aldrich
Phagocytic dysfunctions:
Leukocyte adhesion deficiency
Chediac hegashi
CGD
CO2
Cl HCO3
Cl
CO2 + H2O
CA
HCO3 + H
H+ + Hb-
HHb
O2
In the lungs, the high conc. of O2 will force the HHb form of Hb to
release its proton, forming a relaxed form of Hb. This proton is
combined with HCO3 to form CO2 and H2O ( via carbonic unhydrase,
CA ). When the reaction goes in this direction, i.e. the red direction,
the effect is called Haldane effect.
In tissues, the high conc. of CO2 will force the reaction to go into
the direction of the black hemi-arrows, an effect known as Bohr
effect.
Statistics
1. Relative risk ( RR ): incidence exposed/incidence non exposed.
2. Relative risk reduction ( RRR ): 1 RR
3. Absolute risk reduction/increase: this is AKA attributable risk.
When we speak about interventional study, the attributable risk will be calculated
as absolute risk reduction ( because the intervention we are doing is supposed to
reduce the absolute risk ), which equal to: incidence of cases incidence of control.
If we speak about exposure Vs non-exposure, then the attributable risk will be
calculated as absolute risk increase, which equals to incidence of exposed
incidence of non-exposed.
E.g. In studying the effect of smocking on lung cancer, the incidence of lung cancer
in smokers is 6/10 and in non smackers is 4/10. The ARR, which is the attributable
risk = 6/10 - 4-10= 2/10, i.e. the smacking has the increased the risk of lung
cancer by 2/10 from the base line of 4/10 to become 6/10.
4. ARP is the attributable risk percent that represents the excess risk in the
exposed population that can be attribute to the risk factor. It = ( Risk in exposed Risk in unexposed)/ Risk in exposed. Also it can be calculated as follows: ARP =
(RR-1)/RR.
5. NNT = 1/ ARR. Absolute risk reduction ( ARR ) is the same good old attributable
risk! Just here we calculate it as 'incidence of non-treated ( control ) incidence of
treated ( experimental group )'.
Obviously, ARR and NNT are calculated in clinical trials.
6.NNH = 1/ ARI. Relative risk increase ( ARI ) is the same good old attributable risk!
Just here we calculate it as 'incidence of exposed ( cases ) incidence of non
exposed ( control )'.
Hirsutism
Increase AA absorption
Involved in gluconeogensis
HMG-CoA reductase
Cholesterol
( insoluble )
7-alpha hydroxylase
Fibrates
Bile acids
( soluble )
Porphyrias
Succinyl-CoA
Glycine
Aminolaevulinic acid
Porphobilinogen
Acute intermittent
porphyria
Hydroxymethylbilane
Uroporphyrinogen
Uroporphyrinogen
decarboxylase
Coproporphyrinogen
Heme
Porphyria
Beez!
B1
Thiamine
B2
Riboflavin
B3
Niacin
B4
Lipoic acid
B5
Pantothenic acid
B6
Pyridoxine
B7
Biotin
B9
Folic acid
B12
Cyanocobalamin
primers . Proofreads.
: leading strand. Proofreads.
Prokaryotes
Pol I: removes RNA primer and replace
it with DNA.
Pol II: repair functions, SOS repair.
Pol III: the main enzyme for
polymerization because it works really
fast and have proof-reading capability.
It synthesizes both leading and lagging
strands
Pol IV, V: repair functions, SOS repair.
RNA polymerases
RNA Pol I: rRNA
RNA Pol II: mRNA
RNA Pol III: tRNA, snRNA
Substitution mutation
Transition
Purine is replaced by another purine
or
Pyrimidine is replaced by another
Pyrimidine
Transversion
Purine is replaced by Pyrimidine
or
Pyrimidine is replaced by purine
PN
Vocal cords
RLN
Cricothyroid
Three nerves:
1. Pharyngeal Nerve supplies all of the muscles of pharynx and soft
palate EXCEPT stylopharyngeus, which receives its intervention from the
9th. The 9th also sensory innervates the pharyngeal mucosa.
2. Superior laryngeal nerve. This nerve has two branches:
I. Internal branch that is sensory and supplies the laryngeal mucosa
above the vocal cords [ piriform recess ]. The superior laryngeal artery
runs with this nerve - be careful during thyroid surgery. BTW: Sensory
innervation below the vocal cords is from the recurrent L. nerve.
II. External branch that supply the cricothyroid. The superior thyroid
artery runs with this nerve.
3. The recurrent nerve (under the aorta) supplies all the muscles of
larynx EXCEPT the cricothyroid and cricoretinoid that open glottis only
muscle behind trachea .