Adrenal Cortex – corticosteroids Gonadotrocorticoids

Corticosteroids o Gonads
 Testicles
1. Mineralocorticoids  Ovaries
2. Glucocorticoids o Sex hormones
3. Gonadotrocorticoids
 Estrogen
Mineralocorticoid  Progesterone
 Androgen
o Aldosterone  Testosterone

Function: Function: menses, breast enlargement, voice change etc.

 Conserve sodium Function: secondary sexual characteristics –

 Attract water confirmation of sexual identity
 Removes potassium
Primary sexual characteristics – sex chromosomes
 Fluid regulation (indirect)
Difference:
(Gets extra sodium then water follows)
Addison’s disease Cushing’s disease
 BP regulation Cushing syndrome
RAAS System Other term, “Adrenal Other term, “Paris
insufficiency” disease”
RAAS → Kidney (renin) → goes to blood → blood
(angiotensinogen) – inactive substance → convert to A1 Other term,
(active substance/weak) → goes lungs → ACE → A2 “Hypercorticolism”
(potent) → goes to 2 receptors
Excess or abundant
1. Vascular area – vasoconstriction steroids
2. Adrenal area – goes to adrenal cortex Absence/low production Cause/Type:
of corticosteroids
Glucocorticoids – stress hormones Cushing’s disease – d/t to
Cause: pituitary adenoma
o Cortisol leading to over-
o Cortisone autoimmune damage stimulation
(adrenal cortex) 80%
Function: Laboratory results:
Idiopathic atrophy of Increase steroids
Lowers prostaglandin adrenal cortex Increase ACTH

 Alleviate blood sugar via glycogenolysis Cancer Cushing syndrome – d/t

Infection hyperplasia/hypertrophy
Unused glucose is stored in the liver (glycogenesis) Surgery adrenal cortex leading to
glycogen (hides in the liver, muscles and fats) Overtreatment – radiation over activity of adrenal
Hypopituitarism cortex
Catabolism – breakdown the it will increase sugar
(Simmond’s disease)
Viscous blood Laboratory results:
Poor circulation Increase steroids
Decrease ACTH
 Lowers immune response by decreasing WBC
migration Iatrogenic Cushing
 Lowers down prostaglandin production Over-use or chronic
 Create sensation of pain and steroid use
inflammation
 Produces mucus in the upper GIT – acts Laboratory results:
like a shield or barrier against Increase steroids
hydrochloric acid which can cause ulcer Decrease ACTH
 Decreases calcium via osmotic diuresis Laboratory results:

Sugar attracts water Decrease steroids

Increase ACTH
1. Increase blood sugar Except simmon’s disease
2. Decrease immune response - Low steroids
3. Decrease prostaglandin - Low ACTH
4. Decrease calcium

Effects of increased steroids

Signs and symptoms: Signs and symptoms: Think of Cushing’s MIO
Weight daily
Low level of SALT, High level of SALT, MIO Reverse isolation
SUGAR, SEX SUGAR, SEX Weigh daily Anti-ulcer
Antiarrhythmic PRN
Salt – hyponatremia and Salt Glucagon PRN/D5W Cushing’s disease
hyperkalemia Anti-convulsant – seizure Radiation
Hypernatremia Anti-neoplastic
Arrythmia Arrythmia If stress, infection,
Cardiac arrest problem Water retention surgery – 2x to 3x dose of DOC: Cyproheptidine
Water loss Fluid excess corticosteroids to prevent (periactin) – lower down
Fluid deficit Hypervolemia Addisonian crisis ACTH production
Hypovolemia HPN (worsened sx of Addison’s
Hypotension Weight gain disease) Hypophysectomy
Dehydration Edema
Weight loss Plethoric skin – thin skin Cushing’s syndrome
Purple striae SOC: adrenalectomy
Cause: hypovolemic Moon face
shock and system failure Buffalo hump Iatrogenic Cushing’s
Truncal obesity Gradually taper intake of
Sugar steroids
Salt/sugar problem
Hypoglycemia
Fatigue and weakness – Sugar
earliest symptoms of Conn’s Syndrome
Addison’s Hyperglycemia
Altered LOC o Primary aldosteronism - other term
Poor circulation
Leukocytosis Muscle wasting o Hyperaldosteronism
Increase sensitivity to Thin extremities o Mineralocorticoid
pain Prone to infection o Common: female
Decrease Stress tolerance Low immune response o d/t adreno cortical adenoma
Hypercalcemia Risk for infection o adrenal cortex tumor
GI upset o over production of mineralocorticoids
Sex Fractures
o excess/abundance of aldosterone
Osteoporosis
Alopecia
Amenorrhea Cause: hereditary or genetically acquired
Sex
Decrease libido
Signs and symptoms:
Changes in distribution of Gynecomastia (male)
hair Masculinization (female) 1. Hypernatremia
Bronze skin Hirsutism 2. Arrythmia
Amenorrhea 3. Water retention
Breast atrophy 4. Fluid excess
Deep male voice 5. Hypervolemia
6. HPN
Management: Management: 7. Weight gain
8. Edema
High sodium high Carbs Diet:
High calorie low sodium Laboratory result:
Low potassium low carbs
Hydration (Increase OFI) low calorie  Increase aldosterone
IVF: D5/D10w/PNSS high potassium  Decrease renin – compensation
Kayexalate – k binder Diagnostic test
Gets K to the blood bring potassium supplements
to GIT or stool potassium chloride  MRI/CT scan/UTZ (confirmatory test)
safest: 10 meq/hr  Biopsy – optional
DOC: HRT of potassium saving
corticosteroids for life give diuretics: aldosterone Screening test
on time inhibitor
 Serum aldosterone level
Take with meals spironolactone  Serum electrolytes
2/3 @ am (aldactone)
1/3 @ pm to mimic Management:
normal function antihypertensive
calcium supplements 1. Low sodium
Side effects: PRN 2. High potassium
 3. Potassium saving diuretic
4. DOC: aldosterone inhibitor Possible insulin

example: spironolactone (Aldactone)

Double wall effect
5. Anti-neoplastic
6. Anti-HPN  cell wall and fat wall
7. MIO  fat preventing insulin to enter cell wall
8. Weigh daily
9. Limit fluid Gestational Diabetes Mellitus
10. SOC: adrenalectomy
o 2nd trimester = BS start to go up
Pancreas o 4 to 6 months
o 1st trimester – fetal organogenesis; ↓ insulin
1. Exocrine function requirement
2. Endocrine function o Maternal hormones – increased Blood sugar
Endocrine function Baby In = macrosomia → cephalopelvic disproportion
leading to cesarean section
o Functional unit: islets of langerhans
Baby Out = WOF: Hypoglycemia
Major cells
Signs and symptoms
 Alpha cells – glucagon (Increase blood sugar)
 Beta cells – insulin (decrease blood sugar)  Cold, clammy skin
 Delta cells – somatostatin (GHIH)  Hypoactive cry
 Hypoactive reflexes
 Weak sucking
Diabetes Mellitus Management:
o d/t beta cell problem (insulin)  Glucose water (dextrose) cup feed/IV
o total absence/↓ production – Type 1  Breastmilk
o ↑ resistance to insulin – type 2
o Chronic metabolic condition of CHO, CHON, fats GDM(Mother)
o Systemic condition
o Increased risk for infection
o Non-curable
o Increased risk for hypertension
o Controllable
o Increased risk for eclampsia/pre-eclampsia
o Preventable
 Baby in: insulin
Type 1 Type  Baby out: OHA (teratogenic except metformin)
Insulin dependent non-insulin dependent
GDM + PCOS = insulin + metformin
diabetes mellitus diabetes mellitus
Diagnostics:

Total absence of b1 cell ↑ age increased risk 1. HgBA1C

Leading cause:
autoimmune damage of B
cells
Hereditary
10% mortality rate
Weight loss
DKA – more common
Common onset: <30y/o
Management:
Insulin for life
Diet and exercise
↓ insulin production o Glycosolated Hgb. Test (best)
↑ resistance to insulin o Check amount of glucose binded to Hgb
o Reflects average blood sugar 3 ot 4
Leading cause: obesity,
lifestyle or diet months
o Confirmation
Weight gain
HHNS – more common Normal: 4 to 6 % HgBA1C
DKA – late sign  DM with good control <7.5% (diagnosed already)
 DM with fair control 7.6 to 8.9%
Common onset: >30y/o
 DM with poor control >9%
Management:
2. OGTT
Diet and exercise  3 days before exam increased CHO diet
OHA – is only effective is  3rd night NPO 6 to 8 hrs.
there is still B cell  4th day (AM) – BS checked 30 minutes before
function and 30 minutes after an intake of glucose
solution (7.5g ogtt) – to establish baseline
Function: Stimulate B
cells and decrease Monitor BS hourly next 3 to 4 hours
resistance due to fats
(anti-obesity) Expected: gradual decline/normalization
  Example: renal calculi, thrombus, embolus,
tumor, BP, anatomical malformation

Intra – renal
Diabetes Mellitus Gestational Diabetes
Mellitus  Direct trauma or internal damage towards
HGBA1C OGTT – confirmatory nephron
OGTT FBS  SLE
 AGN
3. Fasting Blood Sugar (2nd best GDM)  Pyelonephritis
Normal: 70 to 110mg/dl  Nephrotic syndrome
NPO: 6 to 8 hrs  HPN
>140 mg/dl = on 2 or more occasions – DM (+)  Cancer
 Medication
Screening test:  Diagnostic test
 Diabetes mellitus
o CBG (capillary blood glucose)
o Random blood sugar Glomeruli/nephrons – blood sugar threshold
o 2 hours post grandial glucose test
(Normal: 160 to 180mg/dl) – blood sugar threshold
To convert mg to mmol divide 18
>180mg/dl – glomerular damage leading to glucosuria
To convert mmol to mg multiply by 18
Special complication: DM
Signs and Symptoms: Diabetes Mellitus
1. DKA
1. Polyuria – happened d/t osmotic diuresis 2. HHNS
2. Polydipsia – compensatory behavior
3. Polyphagia – cell starvation Diabetes ketoacidosis
4. Viscous blood
o Type 1 DM – total absence of insulin production
5. Poor circulation
→ blood sugar>300mg/dl (cause osmotic
6. High risk for infection/gangrene
diuresis) → total cell starvation →
7. Skin discoloration – darker (poor circulation)
gluconeogenesis → catabolism of CHON and fats
8. Altered sensation
→ ketosis (formation od ketones)
9. Blurred vision (poor circulation)
Problem:
10. Altered organ function
1. Metabolic acidosis
11. Glycosuria/glucosuria
2. Dehydration (Priority)
Complications:
That caused of death is dehydration that can lead to
o Macrovascular complications shock…
 Hypertension 2nd
o Type II (late) uncontrolled
 MI
 Angina pectoris Leading cause:
 CVA
 Aneurysm  Skipped, missed, inadequate dosage of insulin ()
 Peripheral vascular disease  Stress, infection and surgery
Example: buerger’s disease, DVT
o Microvascular complications Diagnostic test:
 Diabetic retinopathy – blindness (Both) o Confirmatory test: serum ketones test/ABG
 Diabetic neuropathy
 Diabetic nephropathy Screening test:

Pathy (damage) o (+) urine ketones

RENAL FAILURE Signs and symptoms:

Pre – renal 1. Ketonemia
2. Ketonuria
 Poor perfusion
3. Kussmaul’s respiration
 Not enough blood, fluid, circulation o Cheyne stokes – brain stem damage
 Dehydration, shock, cardiac arrest, MI, o Biots respiration – brain stem damage
congestive heart failure
o Kussmauls breathing – continuous rapid deep
Post – renal breathing no apnea
4. Acetone breath “fruity breath”
 Obstruction of renal flow 5. GI upset
 6. Sx of dehydration 1. Cellular metabolism (breakdown = nutrients →
energy)
2. Growth and development
HHNS Difference:
o Type II only Hyperthyroidism Hypothyroidism
o Decrease insulin production Common: Grave’s Common:
o Increase resistance disease/thyrotoxicosis myxedema/critinism
o Sugar >600 mg/dl above → massive osmotic
diuresis → massive dehydration shock Myxedema – maturity
Critinism – child
Type II → decrease insulin production (No total cellular (prone to mental
starvation) No need for ketosis, gluconeogenesis, NO acid retardation)
→ >600mg/dl above (2) Major Types: (2) Major Types:

Problem: Dehydration Primary – always think Primary - always think

of thyroid gland of thyroid gland
Leading cause:
Overactivity of TG Underactivity/absent
1. Inadequate fluid replacement activity
2. Stress, infection and surgery Primary cause:
autoimmune response Leading cause:
Confirmatory test:
(inflammation) Autoimmune damage
1. serum osmolarity test Genetics (hashimoto’s disease) –
2. ABG – non acidic Adenoma autoimmune
Hypertrophy thyroiditis
Signs and symptoms: SX and S of dehydration Hyperplasia Atrophy
Over treatment (HRT) Cancer
Management: BOTH Surgery (intentional or
Lab: accidental)
1. Initial management: CBQ Priority: Rapid IVF high T3 and T4 Over treatment –
replacements PNSS decrease TSH radiation/chemo
2. Give insulin – IV administration “clear insulin” (iatrogenic cause)
Example: regular/short acting/rapid acting Secondary – always
3. Recheck blood sugar and potassium think of pituitary gland Lab:
If blood sugar is less than 200mg/dl – change Decrease T3 and T4
IVF temporarily to D5 or D10W temporarily – to Overstimulation Increase TSH
prevent sudden drop of blood sugar
Adenoma Euthyroid: Normal
If potassium is low give potassium chloride
Hyperpituitarism state of thyroid
10meq/dl
4. Continue monitoring of blood sugar and Lab: Secondary - always
potassium Increase T3 and T4 think of pituitary gland
Blood sugar is already stable – change IVF back Increase TSH
to PNSS Under stimulation or
If potassium is already stable stop the no stimulation at all
potassium chloride drip
Atrophy
DKA – DOC: NaHCO3 (antacid) Cancer
Stroke
Thyroid Gland Increase ICP
Surgery
o Neck area
Simmon’s disease
o Anterior to PTG Congenital
o 6 nodules hypothyroidism
Iodine deficiency
Hormones:
Lab:
1. Thyrocalcitonin Low T3 and T4
Function: blood to bone calcium Low TSH

Activates during hypercalcemia Signs and symptoms: Signs and symptoms:

2. T3 – triiodothyronine All is All is

3. T4 – thyroxine fast/increase/elevated/ slow/decrease/down/
Sympathetic Parasympathetic
Normal function:
Except for one diarrhea Except for one lugol's solution – Side effects:
(para) constipation (sympa) decrease the size and hyperthyroidism
vascularity of thyroid Take on morning
Increase HR, RR, temp, Decrease BP, HR, RR, gland Before meal
BP, metabolism, Temp, activity, energy,
peristalsis, high level metabolism, peristalsis best: before surgery
energy, activity
Cold intolerance WOF: allergy (seafoods)
Palpitations Initial symptoms: CBQ
SOB/DOB Fatigue Normal flushing and
Intolerance to heat Weakness metallic taste but
Hypertension Decrease appetite monitor it
High appetite Anorexia
Weight loss Weight gain DOC: Anti-Thyroid
Diarrhea Increase cholesterol drugs – lower t3 and t4
Insomnia Constipation production
Initial symptom: Hand Decrease LOC
tremors Lethargic Ex. Tapazole,
Increased of TG = goiter Decrease tolerance to methimazole, PTU
Risk for airway stress and sedatives
obstruction Less active oil glands Side effects: think of
Exophthalmos – Brittle hair and nails hypothyroidism
dalrimpyle’s sign Dry, scaly skin Adverse effects: sore
(thyroid stare) reddened Goiter throat and fever
eyes in frequent
blinking SOC: thyroidectomy –
Fine straight hairs subtotal
Soft smooth skin
Breast enlargement WOF: airway
Jefrey’s sign – forehead obstruction
remains smooth even
when you looked up
Pliable nails
Active oil glands
Lid lag sign – von
graefe’s sign
WOF: thyrotoxic crisis WOF: myxedema coma
“thyroid storm” Adult
Worsened signs and
symptoms

Early symptom:
constant elevation of
heart rate and
temperature

COD: cardiac arrest

Management: Management:
↑ CHO, ↑ calorie, CHON
Low fiber Low calorie, CHON,
No stimulants CHO high fiber

Place the patient in a Warm clothing

cold comfortable/low Warm environment
stimuli room Iodine replacement
PRN
Hydration is needed Steroids PRN
Artificial tears GCS
Lubricating eye drops Frequent bed rest and
Steroids PRN rest periods
Radiation PRN Equally divide
ET set activities
BVM @ bed side Laxatives PRN
Anti-HPN (propranolol) Moisturizing lotion
beta blocker – decrease
BP and control DOC: HRT of thyroid
palpitations hormone for life
 11. Calmoseptine (calamine + zinc oxide) after
procedure
Oncologic Disorder 12. Hyalorunidase – for hydration
13. Alovera
o Radiation treatment
 Treatment and diagnostic purpose Burns
First Superficial Epidermis Pain is
(3) MAJOR TYPES OF ENERGY
degree decrease via
 Alpha particles – weakest form of energy (least cool air
with pain
potent)
Redness
 Does not cross the skin area
(blanching)
 Internal radiation (unsealed) either Swelling
ingested or injected Dryness
 Beta particles – more potent than alpha (but not Pilling
stronger than gamma) Sunburn
 Does not cross skin Second Partial Epidermis, Redness but
 Internal radiation (sealed) degree thickness dermis, with
 Brachytherapy subQ presence of
 Gamma particles – Strongest form of energy with pain blisters
 Crosses the skin
 External radiation (most Most painful
painful) burn
EXTERNAL RADIATION
Wet or moist
o Teletherapy area
o External gamma beam
o Gamma particles Swelling
Machine: Linear accelerator Third Full Epidermis, Dry
degree thickness dermis, Leathery
During treatment: subQ, gray
fascia and Leathery
1. should be on radiation treatment room muscle brown
2. (+) contact radiation precaution Painless
3. (-) body fluid precaution Muscle
4. Pregnant nurse bawal contractures
5. Pregnant nurse + lead apron + gown bawal parin Fourth Deep full Epidermis, Dry
– teratogenic degree thickness dermis, Leathery
SubQ, gray
Lead toxicity – plumbism (Neurotoxic)
fascia, Leathery
6. Post procedure put the patient on the private
muscle, brown
room/single room bones Painless
Muscle
contractures
Isolation Reverse isolation
Infectious Risk for infection patients Sometimes
Safety issues whitish
Solo Positive pressure pushes appearance
air outside the room
Negative pressure pulls With
air inside the room Positive pressure protects presence of
the patient by pushing eschar
the air outside

7. Reverse isolation 14. Do not erase markings – serves as a landmark of

the radiation
Post procedure:

8. (-) contact radiation precaution

9. (-) body fluid precaution

WOF: radiation burns “superficial burns” first degree

burns

10. Avoid any topical or skin products before or

during the procedure – lessen the effectivity of
radiation
 2. Schilling’s test – radioactive vitamin b12
3. Test “scan” except CT scan
o Thallium scan
INTERNAL RADIATION o Renal scan
o Ventilation perfusion scan
A. Sealed o Bone scan
o Beta particles o Fibro scan
o Intracavity 4. RAIU – diagnostic for hyper and hypothyroidism
o Invasive procedure and thyroid cancer
o Also known as brachytherapy or internal radium Patient will drink radioactive iodine then blood
implant or cesium/cervidil implant draws after if there is presence of RAIU
o Implant of seeds, ribbon, beads o (-) or low RAIU blood level
HYPERTHYROIDISM increase RAIU
Nursing consideration: uptake – causes hot nodules
o (+) or high RAIU blood level
1. CBR with NBP HYPOTHYROIDISM or thyroid cancer
2. Catheterization decrease RAIU uptake of the thyroid
3. Diet: low fiber gland – causes cold nodules
4. Bed side: long forceps/long tongs/lead container
5. Code yellow or code orange – biohazard
6. (+) contact radiation precaution
7. (-) body fluid radiation precaution

CBQ Follow the ALARA PRECAUTION

(AS LOW AS REASONABLE AMOUNT OF EXPOSURE) –

protection of medical workers and visitors

Principles:

1. TDS should be followed (time, Distance,

Shielding)
30mins per shift
5mins per visit
6 visits
2. 3 to 6 feet away the farther the better
3. Shielding – lead gown or shield
4. Wear a dosimeter film badge – record and
measures the amount of exposure to radiation
5. Place a precaution sign @ the door and bed of
the patient

B. Unsealed
o Ingested/injecting
o Diagnostic test/treatment use
o (+) boy fluid precaution
o (-) contact radiation precaution
o Remain in the body for 48 hours – 2 days
Management:

1. Flush toilet more than twice

2. Hydration
3. Check KFT before and after

Radioactive iodine treatment: sodium iodide

131 is injected and it will destroy cancer in the
thyroid nodules or it will destroy hyperactive
thyroid nodules
Diagnostic test:

1. Barium swallow (upper GI series)

  In front of mirror
 Circular motion
 Wave like
 Wedge/clock method: BEST
 Outer to inner movement: best but
Breast cancer either will do
 When lying down = place a pillow at the
o Most common type for women
back of the shoulders
o Leading cancer for women the cervical and
2. Clinical breast examination
uterine cancer 3. Mammogram
o Women > men 1%
 With discomfort
Leading cause:  Avoid any topical or skin product before
the procedure
 hormonal imbalance of estrogen
 genetics – used of tumor marker/cancer When is the first mammogram schedule?
markers “Blood test” → BRCA1
It depends, when there is history of breast cancer
 allele is the gene that is passed down
 life style and diet Start 10 years earlier from the age of the relative
 stress that was diagnosed and repeated annually
 early menarche: 9 to 13 y/o
 late menopause: 45 to 50 y/o o Not less than 25 not more than 45
 obesity → PCOS
 OCP – increased risk If no family history

what is the BMI of an individual at risk for breast 35 to 39 years old = base line Only once
cancer? 40 to 49 years old Every 2 years done
Normal: 18 to 24.9 Above 50 Annually
Obese: anything above 30 Common site: metastasis
Signs and symptoms:
o Lungs
1. Painless lumps/dimpling: earliest sign o Bones
2. Orange peel skin “peau de orange”: late sign o Brain
3. Mastodynia – painful breast o Liver
Capsulated, well-defined, movable → Higher chance of
Management:
benign

Asymmetrical. Non-capsulated, non-movable → Higher

1. Radiation
chance of malignant 2. Chemotherapy
3. Surgery: mastectomy more than 7cm
Other signs and symptoms:
Types: Mastectomy CBQ
4. Abnormal nipple discharge
5. Significant physical changes in nipples and 1. Simple mastectomy/total mastectomy
areola o Breast tissue affected with lump
6. Anemia o Areola
7. Weight loss
o Nipple
8. Breast asymmetry
2. Radical mastectomy
Confirmatory test: o Breast tissue affected with lump
1. BIOPSY – confirmatory
o Areola
o Nipple
Screening test: CBQ o Lymph nodes
1. BSE o Pectoralis muscle
 Monthly 3. Modified radical
 7 to 10 days post menses o Breast tissue affected with lump
 Same day each month o Areola
 Both standing up and lying down to o Nipple
check for significant changes o Lymph nodes
 Best time during shower
4. Partial
 o Removal of breast lump but with 2 3. Bladder distention and discomfort
to 3 cm of normal tissue around the 4. Dysuria
mass 5. Hematuria
6. Urinary frequency
7. Increase risk for infection
Most common side effect/complication: Complications: renal failure (post renal) and
Lymphedema (elevate the affected arm) prostate cancer
Drug of choice: Tamoxifen (nolvadex) – anti- Management:
estrogen/hormone modulator
1. Catheterization
o Cytostatic – prevent cell replication or 2. Anti-hypertensive drug (alpha adrenergic
mitosis blockers) – peripheral acting vasodilator
o Used in combination with other treatment OFF LABEL EFFECT it relaxes bladder
modality sphincter
o Side effect: Bone pain (expected) if severe “zosin”
deep bone pain persists consult MD WOF: orthostatic
o Adverse effect: osteoporosis hypotension/postural hypotension –
o Expect also hot flashes risk for injury and falls
o Average intake: 5 to 10 years only Wait fir 3 to 5 mins before changing it
3. Radiation treatment
Benign prostatic hypertrophy
4. Chemotherapy PRN
o Enlargement of prostate gland 5. Diuretics
o Most common Genito-urinary reproductive 6. DOC: Finasteride (Proscar) – anti
disorder of male testosterone/decreases the size or shrink the
prostate glands
o Non malignant
o Non-cancerous 7. SOC: prostatectomy
Most common: TURP
Prostate gland – below the bladder adjacent to the after TURP post procedure Continuous bladder
testicles irrigation is needed to remove clot and debris

Normal function of prostate: alkaline fluid of semen Cervical Cancer

Leading factor: Leading cause: genital warts that cause HPV infection

 trauma
o Hormonal balance of testosterone
 increased risk for HPV: multiple sex partners
o Genetics
 genetics
o Life style and diet  lifestyle and diet
o Medications
o Over use and under use common complication: uterus, ovaries and bladder

0 today > April

Diagnostic test:
1 or 2 months after? > May or June
1. PSA Test (blood test) – prostate specific
antigen 6 months > October
o Normal: <4 mg/ml
Vaccines: Female and Males
2. Cystoscopy
3. CT scan/MRI/UTZ 1. Gardasil – prevent type 6, 11 (rare strain) 16 and
4. Urinalysis 18 (common strain)
5. KFT Quadrivalent vaccine
6. Digital rectal examination – annual starting 2. Cervarix – prevent type 16 and 18
above 4o years old Signs and symptoms:
Signs and symptoms: 1. Initial symptoms: unusual bleeding or discharge

1. Initial symptoms: decrease force and Other signs and symptoms:

amount of urinary stream/Dribbling of
2. Lower abdominal pain
urine
3. Foul discharge
2. Urine retention
 4. Dyspareunia Cause: due to SSRI’s + St. John’s Wort (herbal drug) for
5. Abdominal cramps mood stabilization and also SSRI’s + other anti-
6. Anemia and weight loss depressants
7. Infertility
8. Pain Should not be taken together.

When you are about to shift your medication, you need

to stop the current anti-depressants for at least 1 to 2
Screening test: Pap smear weeks.

 18 years old and above

 <18 years old – sexually active
- Confusion
 Annually
- Hyperstimulation
Confirmatory test: BIOPSY - Agitation
- Muscle rigidity
Management:
Best time to take: AM to prevent insomnia
1. Radiation
2. Chemotherapy II. TCA – second line of drugs
3. Cryosurgery o Elevates serotonin and norepinephrine
4. Conization: removal or cervix If planning to o Teratogenic
get birth o Ask for LMP
5. TAHBSO – if planning to get pregnant
WOF: Teratogenic, cardiotoxic
Anti – depressants medications (Thymoleptics)
o Tachycardia arrythmia – CHF
I. SSRI – first line of treatment
o Drowsiness
o Safest of all anti-depressants
o Only increase one neurotransmitter – Antidote: Physostigmine
serotonin
Examples:
Patient major depression, SAD, postpartum
depression/blues 1. Sinequen (Pamelor)
Side effect:
2. Elavil (Ludiomil) – most
cardiotoxic and most teratogenic
o sodium loss (geriatrics)
o Sexual dysfunction
3. Anafranil (Asendin)
4. Tofranil (Norprmain)
Off label effect: stabilizes other neurotransmitters
Best time to take: PM to prevent insomnia
If high GABA may lead to narcolepsy and comatose
III. MAOI’s – third line
If low GABA may lead to anxiety, seizures ang o Increase serotonin, Norepinephrine,
agitation dopamine
o Most dangerous type
If high dopamine led to schizophrenia and
psychoses Best time to take: AM to prevent insomnia

If low dopamine led to Parkinson’s and dementia Contraindicated: MAOI’s + Tyramine rich food

Adverse effect: Hypertensive crisis

Examples:
Systolic: >160
1. Fluoxetine (Prozac)
Diastolic >110 + neurological manifestations
2. Paroxetine (Paxil)
3. Escitalopram (Lexapro) DOC: Phentolamine (regitine)
4. Citalopram (celexa)
Contraindicated:
5. Sertaline (Zoloft)
1. Aged cheese
6. Fluvoxamine (Luvox)
Except cottage and cream cheese
WOF: Serotonin syndrome 2. Pickled
3. Wine
4. Preserved foods
5. Beans
 6. Avocado DOC: haloperidol (Haldol) - (anti-psychotic) –
7. Banana neuroleptic/major tranquilizers
8. Caffeine
 Removes psychotic symptoms
Examples:
Teratogenic
1. Parnate (tranylcypromine)
2. Marplan (isocarboxacid) Half life (24hrs)
3. Nardil (Phenylzine) 1st week to TSL is unstable (check every day for the 1st
week)

Urine dysfunction (moderate/adequate na intake) 2 to 3

g/day
2 to 4 weeks before achieving the
therapeutic effect Metallic salty taste (normal) informs the patient
Lithium toxicity:
First 1 to 2 weeks (high risk for suicidal
attempts) – needs close monitoring to the Management:
patient 1. Hydration of PNSS
When is the highest risk suicide? 2. Gastric lavage (activated charcoal)
3. Hemodialysis
o First 1 to 2 weeks of anti-depressants
o Monday is the DAY If toxicity: mannitol, kayexalate (Na polystyrene)
o Early morning or dawn
o Month: April to May – strong sunlight (increase
serotonin)

Lithium

o Anti – manic medication

o Bipolar problem – manic depressive
disorder/euphoria dysphoria disorder

Reaction formation – opposite reaction

e.g., sad and happy etc.

Mania – mask of depression

 Initial feeling: sadness

Normal mania: 7 days with at least 3 or more manic

symptoms after 7 days depression will enter

Hypomanic

 4 days mania
 3 or more symptoms

Level – therapeutic serum level (Normal: 0.6 to 1.2

meq/L)

1 – 2 weeks before achieving the therapeutic effect

Lithium is not effective for acute mania

But can prevent future mania (maintenance drug)

Acute mania

DOC: Benzodiazepines/Barbiturates – both elevates

GABA