Type

1 Diabetes Mellitus

Etiology Pathophysiology CM’s

- Environmental 1. Genetic/Environmental - Polydipsia
- Immunological - Polyuria
- Genetic - Polyphagia
- Weight loss
2. Activation of Macrophages, T
- Fatigue
cytotoxic cells, &
autoantibodies toward beta - Hyperglycemia
cells
3. Destruction of beta
cells with decreased
insulin secretion

Type 2 Diabetes Mellitus

Etiology Pathophysiology CM’s
Exact 1. Genetic 1. Obesity - Polyuria
Etiology is 2. Decreased activity of - Polydipsia
2. Decreased Activity of
UNKOWN
Amylin Ghrelin - Polyphagia

- Fatigue
Risk 3. Decreased beta cell 3. Insulin Resistance - Pruritus
Factors: mass and function - Recurrent
Genetic 4. Hypoinsulinemia 4. Increased demand for Infections
Obesity insulin synthesis leads to
Hyperinsulinemia
5. Increased Glucagon 5. HIGH BLOOD SUGAR

6. HIGH BLOOD SUGAR

 Diabetes Insipidus (DI)
Etiology Pathophysiology CM’s
Neurogenic: 1. Decreased ADH secretion/ Insensitive - Polyuria
Head surgery ADH receptor in Kidney - Polydipsia
Brain tumors 2. Nephron does not absorb water - Poor Skin Turgor
Nephrogenic: 3. Body losses high amounts of water in - Dry mucous
Renal the Urine membranes
- HypOtension
4. Dehydration &
Tubular
defect - FVD (fluid volume
Genetic deficit)
Drugs Hypernatremia -
-
HypERnatremia
HypERosomolaity

SIADH
Etiology Pathophysiology CM’s
- Head 1. Excessive ADH Secretion - Edema
trauma 2. Fluid Retention by Kidneys = Edema - Weight gain
- Tumors - JVD
- Infection
- stroke 3. Dilutional -
-
Crackles
Decreased
- Emphysema urine output
- Meningitis
Hyponatremia - HypOnatremia
- HypOsmolaity
- Hypertension







 HypOthyroidism
Etiology Pathophysiology CM’s
- Congenita 1. Loss of Thyroid Function - Fatigue
Thyroid 2. Decrease production of Thyroid - Weight Gain
defects hormone (TH) - Constipation
- Autoimmune: 3. Increase production of TSH - Delayed
Hashimoto Reflexes
disease
- Surgical
4. Slows Basal - Feeling Cold
- Sluggishness
removal
- Thyroiditis
Metabolic Rate

CHRONIC COMPLICATIONS OF DIABETES***

- MICROVASCULAR DISEASE – DISEASED CAPILLARIES (ANGIOPATHY)
o DIABETIC RETINOPATHY – BLINDNESS
o DIABETIC NEPHROPATHY – KIDNEY FAILURE
o DIABETIC NEUROPATHIES – NERVE DAMAGE/LOSS OF SENSATION
- MACROVASCULAR DISEASE – DISEASED ARTERIES
o CARDIOVASCULAR DISEASE – CAD, ANGINA, MI
o STROKE – ISCHEMIC TYPE
- PERIPHERAL VASCULAR DISEASE
o ULCERATIONS, GANGRENE, AMPUTATIONS, INFECTION, IMPAIRED
IMMUNITY, HYPOXIA, DECREASED PERFUSION, DECREASED SENSATION,
DELAYED WOUND HEALING

HypERthyroidism
Etiology Pathophysiology CM’s
Grave’s 1. Body produces TSI or gland enlarges - Nervousness
Disease: 2. Elevated T3 & T4 - Weight loss
Autoimmune 3. Negative Feedback inhibition of Pituitary TSH - Hyperactive
stimulation 4.Low TSH more hormone secreted Reflexes
of thyroid - Diaphoresis
5. High Basal Metabolic
-Toxic - Tachycardia
Adenoma - Increased
-Toxic Rate Systolic BP
Multinodular - Expothalmos
goiter
Normal feedback loops for thyroid and parathyroid***
 Pheochromocytoma
Etiology Pathophysiology CM’s
Catecholamine 1. Excess stimulation of Alpha & Beta - Hypertension
secreting adrenergic receptors - Headache
tumor of the 2. Increased secretion of epinephrine & - Tachycardia
Adrenal norepinephrine - Palpitations
Medulla - Diaphoresis
3. Increased peripheral

vascular resistance

Cushing Disease
Etiology Pathophysiology CM’s
ATCH Dependent: 1. Loss of feedback control of ACTH - Obese trunk
- Pituitary secretion - Moon Face
adenoma 2. Constant secretion of ACTH - Buffalo Hump
- Ectopic secreting - Hirsutism
non pituitary 3. Increase secretion - Ecchymotic
tumor (small cell
in lung of Cortisol areas
- Purple Striae
- Administration - Hyperglycemia
of exogenous
steroids
(syndrome)



 HypOparathyroidism
Etiology Pathophysiology CM’s
Damage or 1. Destruction of gland - Muscle cramps
removal of 2. Insufficient PTH secretion - Irritability
Parathyroid 3. Decrease in Ca2+ levels - Tetany
Gland - +Trousseau

4.Low ca2+
sign
- +Chvostek's
sign

DKA
Etiology Pathophysiology CM’s
- Illness 1. Insulin deficiency + Glucagon excess - Kussamaul
- Stress 2. + blood ketones 2.+ Blood glucose respiration
- noncompliance 3.Acidosis 3. Osmotic diuresis - Nausea and
with insulin 4. Fluid and vomiting
administration electrolyte depletion - Abdominal
pain

5. Cellular dysfunction (occasionally)
cerebral oedema - Fatigue
shock - Thirst
- Sweet smelly
breath
- Confusion
drowsiness
- Hypotension
- tachycardia
 Addison Disease
Etiology Pathophysiology CM’s
Autoimmune 1. Autoimmune destruction of Adrenal Cortical - Bronze
destruction Cells Pigmentation
of Adrenal 2. Adrenal Atrophy - GI disturbances
Cortical Cells 3. Decreased - Weakness
4. Inadequate
- Weight loss
Cortisol causes corticosteroid - Postural
increased and Hypotension
ACTH mineralocorticoid
Synthesis

Rheumatoid Arthritis
Etiology Pathophysiology CM’s
Unclear 1. T lymph activation 1. B lymph Activation -Symmetrical pain in
Higher in 2. RANKL increases 2. Rheumatoid factor small joints
women is formed and binds -Swelling
with IgG -Warmth
Autoimmune 3. Forms Pannus 3. Inflammatory -Erythema
response -Anorexia/fatigue
-Ulnar Drift
4. Destruction 4. Enzymes destroy
-Swan Neck
collagen
of cartilage 5. Forms Pannus Deformity
-Boutonniere
and bone
deformity
6. Destruction of
cartilage and bone
 Osteomyelitis
Etiology Pathophysiology CM’s
1. Entry of Pathogen and inflammatory - Bone pain
Staphylococcus response - Malaise
Aureus 2. Pus accumulation in bone - Headache
- Fever
3. Bone cells become Ischemic

4.Sequestra forms (dead bone tissue) - Edema
5. Involucrum: new bone formation - Erythema over
bone
6. Allows sinus tracts to develop - Brodie
and spread disease Abscess

Gout
Etiology Pathophysiology CM’s
1. Body unable to metabolize Purine - Sudden onset
Familial 2. Leads to increase Uric acid in blood of Asymmetric
3. Uric acid crystals form Joint pain
Diet 4.Deposits into joints usually great
toe
5. Inflammatory response - Edema
- Warmth
- Erythema
- Elevated uric
acid
- Fever

 Osteoarthritis
Etiology Pathophysiology CM’s
Risk Factors 1. Loss of Articular Cartilage - Asymmetric joint
2ndary: pain increases w/
2. Inflammatory Response
activity
- Age, 3. New bone formation of joint margins - Relieved by rest
Obesity (bone spurs) - Heberden’s
- Injury 4.Subchondral bone changes Nodes (DIP)
- Repetitive - Bouchard’s
trauma 5. Synovitis & thickening of joint Nodes (PIP)
Primary: capsule
- Idiopathic

Osteoporosis
Etiology Pathophysiology CM’s
1. Decreases Estrogen - Decreased height
Primary: - Compression
2. Increase RANKL
spinal Fx
- Postmenopausal 3. Bone resorption is greater than - Kyphosis
Secondary: bone deposition - Decrease bone
- Other 4.Alterations in bone mass
conditions Microarchitecture measurements
5. Loss of bone Mineralization - Pathologic
fracture
6. Diminished bone Mass and
Porous bone

PAGET DISEASE= PATHO ONLY****

- CHRONIC ACCELERATED REMODELING OF SPONGY BONE AND DEPOSITION OF DISORGANIZED BONE
o ENLARGES AND SOFTENS AFFECTED BONES
o MOSTLY AFFECTS VERTEBRAE, SKULL, SACRUM, STERNUM, PELVIS, AND FEMUR
KNOW THE DIFFERENCE BETWEEN A SPRAIN AND STRAIN
- STRAIN
o TEARING OR STRETCHING TO A TENDON OR MUSCLE
- SPRAIN - TEAR OR INJURY TO A LIGAMENT


Chronic renal disease

Etiology Pathophysiology CM’s
- Diabetes 1. Renal Injury - Oliguria
Mellitus (MC) 2. Increased release of Angiotensin II - Anuria
- Intrinsic 3. Increased glomerular capillary HTN - Anemia
Kidney Dx 4.Increase in glomerular permeability - Pruritus
- HTN 5. Proteinuria - Uremic Frost
- Cystic Kidney 6. Tubulointerstitial Injury - HTN
Dx
- Atherosclerosis 7. Renal Scarring
- SLE (lupis)

Glomerulonephritis
Etiology Pathophysiology CM’s
- Immunologic 1. Glomerulus injured from antigen- - H/A
(MC) antibody complexes - Malaise
- Drugs/Toxins 2. Precipitates inflammatory process - Weight Gain
- Vascular 3. Inflammatory mediators damage - HTN
disorders basement membrane of glomerulus - Facial Edema
- Systemic - Proteinuria
Diseases
4.Degenerative changes affect - Hematuria
- Viral causes all renal tissue - Oliguria
- Dysuria


 Acute cystitis
Etiology Pathophysiology CM’s
- Escherichia 1. Exposure to Pathogen - Frequency
Coli (MC) 2. Pathogen Travels Upward - Dysuria
- VUR - Urgency
- Cather 3. Causing - Lower abdominal
Indwelling inflammation &/OR suprapubic
Obstruction pain
- Lower back pain
Elderly: may experience
confusion and lower
abdominal pain

Pyelonephritis
Etiology Pathophysiology CM’s
- Bladder 1. Exposure to Pathogen - Fever
infection 2. Pathogen ascends from lower urinary - Flank Pain
- Indwelling tract or bloodstream - Chills
Catheter 3. Inflammatory process developes - Dysuria
- Renal 4.WBC infiltration - WBC’s in the
stones urine
- VUR 5. Inflammation of renal - CVA
Parenchyma tenderness
- Urgency
- Frequency



 Acute kidney injury
Etiology Pathophysiology CM’s
Pre Renal 1. Initial phase: - Oliguria
- Impaired Injury to kidney - Anuria
Renal Blood 2. Oliguria phase: - FVE (edema)
flow Decreased GFR Decreased urine - HTN
Intrarenal: formation - Elevated
- Acute 3. Increased in serum creatinine and BUN creatinine/BUN
Tubular 4.Recovery Phase: - HyperKalemia
Necrosis Glomerular Function Returns
Postrenal: 5. Urine output high but not
- Urinary concentrated (Diuresis)
Tract
Obstructions
6. Recovery Phase:
Healthy Nephrons begin to
compensate

Renal calculi
Etiology Pathophysiology CM’s
- Dehydration 1. Supersaturation of one or more Salts - Pain in Flank
- Diet 2. Precipitation of the salts from a liquid to & abdomen
- Occupation a solid state - Nausea
- Gender 3. Temperature and pH changes - Vomiting
- Age - Cool, Clammy
- Geographic
4. Growth of stone through skin
location crystallization or aggregation - Hematuria





Know the renal lab tests, what they measure, which are most
specific***
- Creatinine is a by product of skeletal muscle contraction and
fluctuates very little, unless kidney prob- if high you move to
GFR 24 hour urine
• Plasma creatinine concentration- 0.7-1.2mg/dL
- BUN les specific- dehydration shows fluctuation
• Blood urea nitrogen (BUN)- 10-20 mg/dL
- Urinalysis- UTI, Blood in urine,
• GFR- 90mL/dL - The filtration of the plasma per unit of time
Know the functional loss of nephron’s with End Stage Kidney
disease****
- GFR less than 15
- Increased BUN 180 – 200 mg/dL
- FVE decreased GFR and activation of RAAS
- Electrolyte imbalance- retention of K, Mg, Phos
- Uremic Syndrome -confusion, anorexia, N/V, pruritis,





GERD
Etiology Pathophysiology CM’s
1. Weakened LES (lower esophageal sphincter) Dysphagia
Older age / increased intra-abd pressure Heartburn
Medications
2. Stomach contents reflux up into esophagus Epigastric Pain
Nicotine
Obesity 3. Acidic juices irritate epithelium and erosion Asthma attacks
Hiatal Hernia 4.Repeat injury causes metaplasia eptithelial Dry Cough
cells Water Brash

5. Barrett’s Espophagus

Peptic ulcer disease

Etiology Pathophysiology CM’s
- H. Pylori 1. Hypersecretion Of HCL - Epigastric Pain
- NSAIDs 2. Erosion in the mucosal lining of stomach or that occurs 1-4
- Alcohol
duodenum hours after
- Increased
stress 3. HCL diffuses into the stomach wall and meals
- Smoking blood vessels - Intense
4.Parietal cells are damaged gnawing,
burning
5. Inflammatory response - Nausea
initiated - Melaenas



Ulcerative colitis
Etiology Pathophysiology CM’s
- Environmental 1. Inflammation at the base of the crypts - Diarrhea
Factors of Liberkuhn - Bloody stools
- Genetics
2. Inflamation of the Mucosa & - Abdominal
- Altered
submucosa of intestinal wall cramping
Immune
response to 3. Leads to shallow ulcerations and - Weakness
intestinal bleeding - Anemia
infection 4.Abscesses are formed - Low grade
fever
5. Necrosis - Dehydration

- Anorexia

Cholecystitis
Cirrhosis
Etiology
Etiology Pathophysiology
Pathophysiology CM’s
CM’s
Most 1. Obstruction of Cystic Duct - RUQ pain
Gallstones 1. Liver Inflammation Jaundice
common: 2. Distension of the gallbladder - Anorexia
Fatigue
2. Liver Necrosis
Alcohol abuse 3. Compromised blood flow and lymphatic - Nausea
3. Liver Fibrosis Anorexia
Hepatitis drainage - Vomiting
Portal HTN
Autoimmune 4.Developmental or portal HTN - Heartburn
Hepatic 4.Ischemia Ascites
- fever
Obstruction Hepatomegaly
- +Murphy's
Sign



Appendicitis
Etiology Pathophysiology CM’s
Obstruction of 1. Subsequent bacterial infection - Gastric or Periumbilical Pain
the appendix 2. Inflammation - Rebound tenderness to RLQ
lumen
3. Ischemia - Mburry’s Point




4.Necrois

Crohn’s disease
Etiology Pathophysiology CM’s
- Same as UC 1. Chronically inflamed intestinal wall - Diarrhea (MC)
- Enviromental - Abdominal
factors
2. Increase tissue damage leads to Pain
- Genetics
- Altered formation of lesions and ulcers - Vit B 12
Immune Anemia

response to
intestinal
3. “skip” 3. Fissures
infection lesions and Fistulae

(reddish form

purple areas)

HEPATITIS PHASES AND THEIR ASSOCIATED CLINICAL MANIFESTATIONS****
- 1. ASYMPTOMATIC PHASE
- 2. PRODROMAL PHASE
o STARTS 2WEEKS AFTER EXPOSURE
o N/V, VOMITING, MALAISE, ANOREXIA, LOW GRADE FEVER, HA
- 3. ICTERIC PHASE
o STARTS 1-2 WEEKS AFTER PRODROMAL PHASE AND LASTS UP TO 6
WEEKS
o JAUNDICE, DARK TEA COLORED URINE, CLAY COLORED STOOLS,
HEPATOMEGALY, RUQ PAIN
- 4. RECOVERY PHASE
o RESOLUTION OF JAUNDICE 6-8 WEEKS AFTER EXPOSURE
o LIVER MAY REMAIN ENLARGED FOR UP TO 3 MONTHS



Etiology Pathophysiology CM’s
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