Show Menu

Test 2 Cheat Sheet (DRAFT) by

Path - Test 2 for 1068

This is a draft cheat sheet. It is a work in progress and is not finished yet.

Patho - Test 2

Week 4 - AS
Disorders of Arterial Circulation
1. Hyperl­ipi­demia - an increase in blood choles­terol as chol. and tri. increase, so does HD & stroke
2. Athero­scl­erosis - plaque buildup in arteries
3. Occlus­ion­s/O­bst­ruc­tions - complete or partial bloackage in b.v (veins or arteries)
5 Lipopr­oteins
1.Chyl­omi­crons 2. VLDL 3. IDL
4. LDL - too much fat --> liver saturated --> too much in blood --> excess LDL binds to endoth­elial cells --> macrop­hages bind to LDL --> m.p oxidize LDL (key contri­butor to AS)
5. HDL - "­goo­d" & synthe­sized by liver - transports chol back to liver from periphery
*smoking * HTN * family hx * HDL less than 40mg/dL * diabetes
Accumu­lation of lipid-­laden macrop­hages forming a lesion called plaque
Leading cause: CAD, stroke, peripheral arterial disease
increasing age, male, genetic disorders of metabo­lism, family hx of CAD OR smoking, obesity, HTN, HYLIP, diabetes
Pathog­ensis of AS
1. Endoth­elial Injury - smoking, LDL, immune mechanisms & mechanical stress from HTN cause this with adhesion of monocytes and platelets
2. Migration of inflam­matory cells - endoth­elial cells bind to monocytes and platelets that start AS lesions - monoctyes adhere to endoth­elium and stay in intima, transform into macrop­hages and engulf LDLs
3. Lipid Accumu­lation & SM prolif­eration - macrop­hages engulf LDL (protects but contri­butes to AS) & activated macrop­hages release toxic o2 that oxidizes LDL. Oxidized LDL ingested by macrop­hages result in FOAM CELLS
4.Gradual develo­pment of plaque - consists of smooth muscle cells aggreg­ation, macrop­hages, ECM, lipids. Superf­icial fibrous cap = SMC's and dense ECM
Plaque Structure
shoulder consists of macrop­hages, SMC's & lympho­cytes
Central core = lipid laden foam cells and fatty debris
Rupture or erosion of unstable fibrous cap can lead to hemorrhage into plaque or thrombotic occlusion in vessel lumen
STABLE thick fibrous cap, partially blocked vessels, no clot formation or emboli
UNSTABLE thin fibrous cap, completely block artery, can rupture = thrombus or embolus

Week 6 - Cerebr­ova­scular Disease

Tissue Perfusion: process of blood to a cap. bed in tissue "pour over or throug­h" - blood flow
Aneurysm abnormal bulging of arterial wall, worsens over time as blood pushes against it, eventually bursting
Ischemia: low flow of blood to tissues and causes damage to target tissues (via obstru­ction or hemorr­hage)
Embolism blockage forms clot and moves through circ.
Stroke: acute focal neurol­ogical deficit from vascular impairment of cerebral blood flow (> tissue perf & ischemia --> neurol­ogical deficits)
2 types ISCHEMIC (caused by thromb­osi­s/e­mboli) & HEMORR­HAGIC (subar­achnoid anuerysmal hemorr­hage)
Ischemic Stroke
risk factors: HTN, smoking, diabetes, carotis stenosis, sickle cell diease, hyperl­ipi­demia, atrial fibril­lation
5 stoke subtypes: 1. large artery AS disease, 2. small vessel or pen. artery, 3. cardio­genic embolism 4. crypto­genic stroke 5. unusual causes
Penumbra central core of dead/dying cells surrounded by ischemic band of cells called "­pen­umb­ra" HALO.
cells inside penumbra experi­ence: impaired metabolic activity, eletrical failure, structural intg. cells maintained
Survival is dependant on return of circ.
will remain viable for several hrs due to collateral arteries supplying the zone
LARGE vessel (throm­botic) Stroke
thrombi most common cause of ischemic stroke in AS vessels (common sites: internal carotid, veterbral arteries, junctions at basilar and vertebral, arterial bifurc­ations)
Affects - cerebral cortex as APHASIA & neglect as VISUAL & UNILATERAL
SMALL vessel (lacunar infarct) Stroke
small infarcts located deep in brain result from occlusion of smaller penetr­ating branches of larger cerebral arteries
- healing lucunar ifarcts leave behind lacunae (small cavities from AS)
Affects - hemipl­egia, dysarthia (weakness of hands), MRI to diagnose
TIA - "­min­ist­roke* where blood flow reverses before infarction occurs (1 hr symptoms), zone of penumbra, caused by AS, warning
Cardio­genic Embolic Stroke caused by moving blood clot that travels from its origin to brain, frequently in middle cerebral artery, originate from heart, SUDDEN
Homonymous Hemian­opsia - food on left side not seen
Diagnosis of Acute Stroke
CT, MRIs, catheter based conven­tional arteri­ogr­aphy, sonography
Treatment GOALS: saving tissue, preventing secondary stroke, min. long-term disability --- reperf­usion tech. like tPA, cathet­er-­dir­ected clot distru­ption, aug. of CPP
Post MGMT highest risk 1 week after stroke or TIA, anti-p­latelet agents, warfarin
- often fatal - rupture of b.v - hemorrhage in brain tissue - compre­ssion in brain tissue by expanding hematoma and tissue edema in brain
most common is aneurysmal subara­chnoid hemorrhage (SAH)
Risk Factors** - age, HTN, aneurysm, trauma, tumors, blood coag. disorders, drugs etc
Manife­sta­tions 1. vomiti­ng/­hea­dache 2. contra­lateral hemiplegia (hemor­rhage into basal ganglia) 3. Edema exert pressure = coma & death (monro­-kellie hypoth­osis)
SAH: arise from congenital defect in medial layers of involved vessels - rupture of aneurysm casues bleeding into SA space leads to increased ICP
Manife­station of SAH BEFORE: asympt­omatic, history of headaches, chronic headache AFTER: sudden headache, LOC, vomiting, blurred vision, sensory deficits, HTN, cerebral edema
Diagnosis: clinical, CT scan, vascular imaging, lumbar puncture
VASOSPASM: involves focal narrowing of cerebral arteries - decreasing neurol­ogical status due to blood loss to area, 3-10 days after rupture
treatment - vasoactive drugs, IV fluid, risk of re-ble­eding, balloon dilation, meds (nimod­ipine)

Patho - Test 2

Week 4 - HTN
o most common health problem
o leading risk factor for CV disorders (creates AS, increases workload on heart in left ventri­cular hypertrophy)
o more men
high BP marked with progre­ssive target organ damage (180/120)
w/ severe headac­he/­cer­ebral edema
Treatment partial reduction in bp to safer level
Special Pops
Pregnancy - precla­mps­ia-­ecl­ampsia
Childr­en/­ado­les­cents - lifestyle or secondary HTN (kidney issues)
Older adults - stiffening of large arteries
Week 4 - Cardiac Conditions
CAD: Heart disease cause by impaired coronary blood flow (AS most common cause)
Pathog­enesis of CAD
no symptoms until advances b/c collateral flow
lesions usually located in LAD and RCA
CAD - 2 types
1. ACS - acute plaque disruption (unstable angina to MI) & presence of ST segment elevation present to confirm, T wave inversion, abnorm. Q wave
Diagnosis of ACS troponin I & troponin T (PRIMARY - rise 3 hr post MI and last 7-10 days), myoglobin, CKMB
2. Chronic ischemic heart diease - AS or vasospatic obstru­ction of coronary artery (ie, stable angina)
Stable Plaque = stable angina
Unstable Plaque = pl. disrup­tion, platelet agg, thrombus, unstable angina & MI
Pathop­hys­iology of MI Occlusion -->­con­tra­cti­bility stops depriving myocardial cells --> LA accumu­lates and fibres irritated --> angina --> lead to MI
Chronic Stable Angina
Angina Pectoris"­sudden attack of angina due to transient myoc. ischemia
STEMI: ischemic death of myocardial tissue occurs when a ruptured plaque blocks a major artery comple­tely. - ST elevation.
Unstable Angina­/NSTEMI: caused by a block in a minor artery or a partial obstru­ction in a major artery. More severe prolonged angina
STEMI - Referf­usion: Reesta­blish blood flow w/fibr­ino­lytic therapy BENEFITS - prevent necrosis, improve mycar. perfusion (recovery called stunned)
Treatment of AMI firbin­olytic therapy, PCI & CABG

Week 7 - Respir­atory Conditions Part 1

cap fluit move to alveoli, hgb leaves = cyanosis, coughing, crackles, tachyc­ardia, cool skin
treatment - non pharm: o2 and assistance with breathing -- pharm: diuretics, ACE inhibitors
presence of air in pleural space, causes partial or full collapse
1. Sponta­neous rupture of bleb on surface of lung, allows air from airways to enter pleural space, higher alveolar pressure and air flows into space, collapse
primary:healthy, belbs at top, smoking
secondary:pt with lung disease, can be life threat­ening
2. Traumatic caused by penetr­ating or non-pe­net­rating chest injuries (fracture ribs)
3. Tension life-t­hre­atening condition where injury allows air to enter but not leave, opposite side compre­ssion, shift in medias­tinum, compre­ssion in vena cava, decrease in venous return to heart and decrease CO
diagnosis - clinical and xray CT
treatment small pnuemo­thr­oaces, o2, need apsiration
HEMOTHORAX presence of blood in plueral space - all same as penuem­othorax
1. Expose to allergin - mast cells release inflam­matory mediators (symp. 10-20 min) 2. Infiil­tration of WBCs - release of cytokins (increased mucous) 3. Bronch­ospasm - caused by stim. of PS receptors, mucosal edema
late phase 1. Inflam­mation and increased airway respon­siv­eness (4-8 hrs after exposure) 2. Release of inflamm. mediators from mast cells (induce migration and basophil activa­tion) 3. Epithelial injury and increase vascular permea­bility (edema) 4. Bronch­ospasm
treatment SABA or LABA, brochi­dil­ators (b2 agonists, antich­oli­nergic agents), steroids, aeroch­amber more effective
COPD (emphysema & chronic brochitis)
-chronic obstru­ction of lung airflow that interferes with normal breathing and not reversible
- not cureable -
emphysema: enlarg­ement of air spaces and destru­ction of lung tissues, a1 deficiency
COB: obstru­ction of small airways, chronic irritation (smoking)
patho increased mucous cells, mucous hypers­ecr­etion, hypert­rophy in glands in trache­a/b­ronchi, imflam­mation, fibrosis bronch­iolar wall, increase goblet cells, viral and bacterial infections
clinical fts insidious onset, cough in am, dyspnea, SOB
manife­sta­tions wheezes and crackles, tripod position, pursed lip breathing, hypoxemia, cyanosis
Emphysema Patho
increased neutro­phils in alveoli secrete trypsin, and imbalance of tryspin and a1 decreases protec­tion, elasrase triggers breakdown of elastin, which damages alveoli
smoke --> inflam­mation --> acti. neutro­phils --> inactiv. of antipr­oteases --> increase elastase activity --> tissue destru­ction
PINK PUFFER - usually emphysema, increases resp to maintain o2, dyspnea, lip breathing BLUE BLOATERS - usually bronch­itis, cannot increase resp enough to maintain o2, cyanosis, cor pulmonale

Week 5 - Heart Failure (CHF)

Heart Failure any structural or functional disorder of the heart w/ low CO &/or pulmonary or systemic congestion
Common Causes: CAD, HTN, dilated cardio­myo­pathy, valvular HD
Heart as a pump
Preload - blood in ventricles at end of diastole right before ven. contract, blood pressure in l. vent. before contra­ction
Afterload - force of contra­cting heart muscles to eject blood, resistance in systole, Afterload created by Arteries
Contra­cti­bility - ability to contract, increases CO, ATP & Ca+
Systolic dysfun­ction decreased contra­cting --> decrease EF (less than 40%)
Manife­sta­tions - increase in preload --> blood accumlates in atria and pulmonary venous system --> pulmonary conges­tions
Diastolic dysfun­ction - inability for l. ven. to fill during diastole.
leads to increased pressure in left atrium --> pulmonary congestion & decrease lung compliance --> CO is decreased bc decreased filling
Frank Starling Mechanism
- end result is increased SV - preload (end diastolic volume) increases - cardiac muscle fibres stretch & trigger stronger contra­ction - increases CV at lower HR
Manife­sta­tions of CHF
1. impaired pumping 2. decreased renal blood flow 3. sympat­hetic nervous system
symptoms fluid retention, dyspnea, fatigue, cyanosis, malnut­rition, arrhyt­hmias
Acute pulmonary edema
cap. fluid moved into alveoli
SEVERE pulmonary edema due to elevated left ventri­cular filling pressures decrease o2 supply to brain, confusion, dyspnea, frothy pink sputum, crackles
Treatment non-pharm: exercise, Na+ & water restri­ctions, weight mgmt
pharm: diuretics, digoxin, ACE inhibi­tors, beta-b­lockers
others - o2, cardiac re-syn­chr­oni­zation, ventri­cular assist devices

Week 8 - Respir­atory Conditions Part 2

TYPICAL: bacterial infection, inflam­mation and exudation of fluid into alveoli ATYPICAL: involves alveolar septum and inters­titium of lung, ourulent sputum, leukicytosis
patho 1. aspiration 2. release of bacterial endotoxin 3. inflam­matory response (neutr­ophils, fibrinous exudate, RBCs) 4. red hepati­zation and consol. of lung parenchyma -- leukocyte infilr­ation -- 5. gray hepati­zation and depo. of fibrin, phagoc­ytolsis of alveoli 6. resolution of infection (macro­phages engulf neutro, fibrin and bacteria
Acute Bacterial (typical) Pneumonia
1. Pneumo­coccal pne. or strept­ococcus pne. - attaches and colonizes to mucosa, delays phagoc­ytosis, acts as antigen
onset malaise, shaking, chills, fever
initial stage cough, watery sputum, fine crackles
progre­ssive cough with purulent blood tinged sputum, lung pain with breathing
elderly = less likely to have temps (may only have loss of apetite or bad mental status)
2. Pneumo­coccal Pne. - vehicle transm­ission, impairs gas exhange, 2-10 days after infection, dirrhea
manife­sta­tions malaise, weakness, lethargy, fever, dry cough
atypical - lack of lung consol­idation and alveolar exudate, less sputum, elevation of WBCS
mycoplasma pne. common bacterial agent in children
TB - slender rod-shaped bacilli that do not form spores
myobac­terium waxy cell wall and respon­sible for: slow growth - ability to trigger immune response - rest. for destru­cti­on/­ant­ibi­oti­cs/lab stains
patho inhaled droplet pass down bronchial tree and land in alveoli, bacilli are phag. by alveolar macro but resist killing, intitiate cell mediated immune response that contains infection, bacilli multiply, infect macrop­haes, degrade myobac­teria and present antigens on helper t lymphs.
INITIAL TB INFECTION - macro begin cell mediated response, results in granul­omatous lesion (GHON FOCUS) containing macro, t cells and inactive TB bacteria
patho cont t helper cells stim. macro to increase and kill mycoba­cteria, when released they damage lung tissue, cytotoxic t cells and macro constitute the cell mediate response that takes 3-6 weeks to become effective
Ghon Focus: area where organisms ends up in lungs turn gray granuloma (typically in upper seg. of lower lobes and lower seg. of upper lobes
Ghon Complex: undergoes soft necrosis, caseous granuloma form along lymph channels, later shrinks, becomes fibrous and calcified, visible with chest xray
primary TB - previous unexposed pt (inhale) - insidious symptoms: fever, weight loss, fatigue, night sweats abrupt onset: high fever, pleuritis and lympth­ade­nitis
secondary TB: reinfe­ction from inhaled droplets or reacti­vation with dry cough, low grade fever, productive blood tinged sputum
treatment of TB - elimin­ating bacilli in infected pt, preventing spread, antibi­oltics (INH and rifampin)

Week 5 - Peripheral Vascular Disease

systemic AS distal to aorta w/ claudi­cation, atrophic change­s/t­hinning of skin, weak pedal pulse, ischemia pain, gangrene, ulcers on toes, ankles
- inspection of limbs, palp, pulses, ankle-­bra­chial index, US, MRI, CT, angiog­raphy
- protection of area, walking to point of claudi­cation, avoidance of injury, antipl­ate­lets, surgery
- manifested by venous HTN, causes reflux in veins, prolonged standing increases pressure and dilated vessel wall
Manife­sta­tions - tissue conges­tion, edema, necrosis of fat deposits, brown pigmen­tation, advanced (stasis dermat­isis, ulcers ankles uneven)
Treatments - compre­ssion therapy, dressings, bandages
DVT or thromb­oph­lebitis
- presences of thrombus in vein w/ imflam­matory response (calf)
risk factors: VIRCHOWS TRIAD (blood stasis, hypera­ctivity of blood coag. vessel wall injury) & increase risk with bad cardiac function
- usually asympt­omatic (if not, pain, swelling etc) U/S, tx is preven­tion, warfarin, IVC filter, compli­cations - pulmonary embolism