Patho Final Exam

lack of vitamin B12

etiology: alcohol overuse, poor nutrition

sequela: macrocytic anemia

s&s: paresthesia, glossitis

lack of vitamin B1

etiology: alcohol overuse

known as: Wernicke-Korsakoff syndrome, a type of beriberi

s&s: problem with memory, ataxia, nystagmus, paresthesia

hypopolarization

lab values: hypocalcemia, hyperkalemia

s&s: muscle spasms, twitching, tetany, positive Chvostek’s sign, tachycardia

hyperpolarization

lab values: hypercalcemia, hypokalemia

s&s: sluggishness, weakness, mental slowness/confusion, bradycardia

normal serum osmolality

280-295

causes of water loss

diarrhea, vomiting, decrease fluid intake

causes of water gain

psychogenic water-overdrinking, too much IV fluid, kidney failure & SIADH that cause retention and low urine output

s&s of systemic inflammatory response

malaise, aches, pain, fever, leukocytosis (neutrophilia), elevated CRP, presence of APR

roles of protective prostaglandins

1. proper clotting

2. stomach lining

3. renal function

4. appropriate vasomotor tone

5. proper immunocyte function

s&s of SIRS

1. altered mental status

2. fever > 100.4

3. increased HR

4. increased RR

5. abnormal WBC count

too little inflammation: two main causes

1. defects in phagocytic function (leukopenia of post-chemotherapy patients)

2. impaired phagocytic function (toxic level of glucose seen in patients with DM affects the immunocyte function)

side effects of protective prostaglandins suppression

1. easy bleeding

2. stomach ulcers

3. kidney problems

4. vasoconstriction

5. infection risk

s&s: local allergic hypersensitivity

dermatitis, nasal allergic rhinitis, conjunctivitis

s&s: systemic allergic hypersensitivity

itching, urticaria, NVD, wheezing, angioedema, HoTN

Tx for systemic hypersensitivity

antihistamines, steroids, leukotriene inhibitors

autoimmune hypersensitivity

patho: autoantibody attacks antigen → immune complex formed → deposited in blood vessel lining of tissues → vasculitis → widespread inflammation

example: lupus

sequela: elevated CRP

sequelae of hemolysis

clogged blood vessels

1. kidney failure

2. ischemia of distal tissues

3. rash

4. fever

5. HoTN

opportunistic diseases

1. harmless flora: thrush, pneumocystis jiroveci, cytomegalovirus, Kaposi’s sarcoma

2. strange organisms: fungus, helminth

when should one use contact precautions?

patient has

1. MRSA

2. diarrhea

3. stool incontinence

4. draining wounds

5. sores

PPE for contact precautions

1. hand washing

2. gown

3. gloves

PPE for standard precautions

1. hand hygiene

2. use of PPE

3. disinfection of surfaces and equipment between each patient use

two types of antibiotic resistance

1. beta-lactamase: enzyme that renders penicillin abx useless. examples: MRSA, resistant strep pneumonia

2. mutation to the pathogen’s cell membrane: vancomycin resistant enterococcus

causes of abx resistance

1. overtreated/overuse of abx

2. inappropriate abx tx (not taking as prescribed/use abx for viral infection)

microcytic anemia

lab values: low RBCs, low MCV, low Hgb

example: iron deficiency

etiologies: heavy menses, GI bleeding

Tx: iron supplements

macrocytic anemia

lab values: low RBCs, high MCV

etiology: disease causes faulty DNA coding of RBC size → RBC is larger than normal (aging, chronic GI problems, alcohol abuse → decreased intrinsic factors → decreased vit B12 → DNA malfunction)

example: pernicious anemia

s&s: fatigue, paresthesia, glossitis, coordination problems

tx: injection of b12

normocytic anemia

lab values: low RBCs, normal MCV

causes: low erythropoiesis, rapid blood loss

Tx: erythropoietin injection

too little clotting

etiologies: thrombocytopenia OR clotting factor deficit

s&s: under skin (petechiae, purpura, ecchymosis), occult bleeding, frank bleeding

too much clotting

etiology: thrombocytosis

sequelae: increased risk for venous or arterial thrombosis & emboli

splenomegaly

→ hypersplenism → sequestration → pancytopenia

etiologies: HTN

atherosclerosis, overdrive of SNS, overdrive of RAAS

S&S: HTN

neurologic: stroke, retinal changes from damage arterioles in retina

renal system: hematuria, proteinuria, renal failure

circulatory system: increased heart workload, MI, HF, PAD, ventricular hypertrophy

Tx: HTN

ACE inhibitors, diuretics, beta-blockers, Na reduction, dietary/lifestyle modifications, smoking cessation, decrease LDL, increase HDL, exercise

s&s: PAD

1. pain (intermittent claudication)

2. pale

3. poikilothermia

4. prolonged cap refill, diminished pulses

5. paresthesia

6. no hair

7. skin ulcers

Virchow’s triad

1. venous stasis

2. injury to endothelium of vein

   1. hypercoagulability

S&S of DVT

s&s of thrombophlebitis: pain, erythema, warmth

S&S of PE

SOB, chest pain, hemoptysis

Tx: venous thromboembolism

encourage mobility and hydration, put up feet, watch for skin stasis ulcers, anticoagulants

sequelae: Afib

diminished CO, arterial thrombi (stroke), venous thrombi (PE)

S&S: myocyte ischemia

chest tightness, heaviness, pain, left arm pain radiates to jaw

stable angina

characteristic: chest pain reduced with rest/NTG

Tx: NTG

compensatory mechanism: collateral circulation

unstable angina

characteristics: plaque rupture which partially occludes the coronary artery, chest pain occurs at rest

s&s: chest pain, diaphoresis, NV

myocardial infarction

characteristics: plaque rupture which totally occludes the coronary artery, chest pain occurs at rest

s&s: chest pain, diaphoresis, NV

Dx: positive troponin

Tx: CAD

1. oxygen

2. NTG

3. other vasodilators

4. anti-hypertensive

5. antiplatelet/anti-inflammatory: aspirin

S&S: left HF

1. pulmonary congestion (lung crackles, dyspnea, orthopnea, PND)

2. poor perfusion

S&S: right HF

1. peripheral congestion (jugular vein distension, hepatic vein congestion, ascites, peripheral edema)

2. poor perfusion

S&S: poor perfusion

1. prolonged cap refill

2. pale

3. poikilothermia

4. fatigue

5. weakness

6. mental status change

7. HoTN

8. low urine output

Diagnosis and Tx of HF

Dx: BNP level (when ventricles are distended, this protein is produced)

Tx: vasodilators, diuretics, positive inotrope

at high risk: aspiration pneumonia

1. elderly patients

2. debilitated

3. unconscious

patho: aspiration pneumonia

pt with high risks will have suppressed gag/cough/swallow reflex, can result in aspiration of food/fluid

patho: general pneumonia

microorganism inhaled → inflammatory reaction → debris collected in parts of lungs → block bronchioles and/or bronchi → atelectasis (collapse of small portions of lungs) → consolidation (stiffened lungs)

S&S: pneumonia

hypoxemia, crackles upon auscultation/area of diminished sound, cough, dyspnea, fever, abnormal chest xray

S&S of high V/Q disorders

SOB, chest pain, hemoptysis, HoTN

patho: high V/Q disorder

embolus lodges in smaller pulmonary arterioles → blood does not get to alveoli → can cause infarct of parts of lung tissue + general hypoxemia

what is the problem with patients with obstructive dz?

elastic recoil of lungs is poor → hard exhalation & often patients must use accessory muscles when exhaling

Tx: obstructive dz

bronchodilators, steroids, smoking cessation, peak flow assessment

s&s: obstructive dz

use of accessory muscle in exhalation, hypoxemia because of decreased gas exchange across narrowed bronchi

patho: asthma

genetic predisposition to have hyper-responsive airways to environmental allergens → inflammation → edema of bronchial lining + bronchial constriction & spasms → narrowed airways

s&s: asthma

wheezing upon exhalation, mild R alkalosis, mild hyperventilation

what if asthma/emphysema gets worse?

cannot hyperventilate → CO2 retention → hypercapnia → R acidosis

etiology: asthma

genetic predisposition to have hyper-responsive airways to environmental allergens

etiology: emphysema

irritants in cigarette smoke

patho: emphysema

irritants in cigarette smoke → inability to expel them due to altered cilia → chronically inflamed airways + elastase (a type of proteolytic enzyme) breaks down the proteins that make lungs elastic → destruction of the alveolocapillary membrane → large, stiff, hyperinflated alveoli with no elastic recoil → air is trapped & becomes harder to exhale it

s&s: emphysema

pink puffers: thin, barrel chest, tripod position, retractions, pursed lip breathing, mild R alkalosis

etiology: chronic bronchitis

irritants in cigarette smoke

patho: chronic bronchitis

irritants in cigarette smoke trigger chronic inflammation → can’t expel CO2 → NO hyperventilating

s&s: chronic bronchitis

cyanotic, no hyperventilating, overweight, finger clubbing, hypoxemia

patients with chronic bronchitis tend to have…

cor pulmonale: right ventricle is unable to get blood into the stiff, full-of-mucus areas

hydronephrosis, then malfunction of nephrons & subsequent renal failure

main serious sequela of any urinary obstructive disorder

benign prostate hyperplasia

at risk: men > 50

biggest problem: urethra is compressed

s&s: urgency, weak flow, slow to start flow, urinary retention

two types of urologic infections

cystitis and pyelonephritis

who is at risk for urologic infections? why?

women, due to short urethra & proximity of urethral meatus to anus & vaginal os

s&s: urologic infection

dysuria, frequency, pyuria, hematuria, costovertebral angle pain, fever

in women, _____ may cause compression of the urethra

uterine prolapse

s&s: acute kidney injury

acute oliguria, acute jump in SCr

etiologies: pre-renal AKI

renal artery blockage, decreased CO from a volume deficit (bleeding, dehydration, HF, sepsis)

etiology: post-renal AKI

obstruction causes backup of urine into kidney (hydronephrosis)

etiology: intrarenal AKI

acute tubular necrosis

etiology: acute tubular necrosis

nephrotoxic drugs, hydronephrosis, toxic microbes, toxins, poisons

s&s: acute tubular necrosis

cast seen in urine

kidney hierarchy

prerenal/postrenal AKI → intrarenal AKI → chronic kidney dz

etiologies: chronic kidney dz

AKI that is not fixed, post-strep glomerulonephritis

s&s: renal dysfunction

oliguria/anuria with low specific gravity, azotemia, uremia, hyperkalemia, hyperphosphatemia, hypocalcemia, M acidosis

why is BUN high in patients with renal dysfunction?

urea nitrogen is a breakdown product of protein, and the kidneys cannot get rid of it. however, only high BUN can’t conclude if the patient is having renal problem.

what kind of test is used to measure serum creatinine?

24-hr urine creatinine clearance to estimate the GFR