quiz 1- CV 1-3 Flashcards
1
Q
• What is atherosclerosis?
A
chronic inflammatory response in walls of arteries, mostly dt deposition of lipoproteins (plasma proteins that carry cholesterol and TGs).
• hallmark is formation of multiple plaques within arteries.
2
Q
• What are the multiple cellular elements involved in development of atherosclerosis?
A
• Endothelial cells, smooth muscle cells, plts, WBCs, many chemotactic and inflammatory mediators.
3
Q
• What is atherogenesis?
A
- result of complex and incompletely understood interactions bw the cellular elements and other biologic processes; lead to signs of atherosclerosis
- Contributors: Vasomotor function, thrombogenicity of vessel wall, state of activation of coagulation cascade, fibrinolytic system, smooth muscle cell migration and proliferation and adrenergic stimulus
4
Q
• What is the “response to injury” theory?
A
- Help explain atherogenesis; endothelial injury is main factor initiating it
- Vascular injury (mechanical, immune complexes, viruses, homocysteine, etc)
- Trap LDL in arterial wall
- Oxidize LDL (oxLDL)
- monocytes/T-cells adhere/migrate into subendothelium
- Monocytes/M0s ingest lipid = “foam cells”
- Foam cell, T-cells, and smooth muscle “fatty streak”
- Continued cell influx and smooth muscle proliferation “fibrous plaque”
- plaque fissure/rupture w activation of platelets and thrombogenesis
- Occlusive thrombi and ischeimic event
5
Q
• What may contribute to endothelial injury?
A
- HTN and cell wall damage from sheer force of blood flow
- ↑ oxLDL, hyperglycemia, hyperhomocystinemia
- infectious agents
- chemical toxins, particularly cigarette smoke.
6
Q
• What do monocytes do?
A
- Circulate, infiltrate intima
- differentiate into M0s, ingest oxLDL
- slowly turn into large “foam cells“
7
Q
• what are foam cells?
A
- Many cytoplasmic vesicles of high lipid content.
* eventually die, further propagate inflammatory process.
8
Q
• What happens to smooth muscle in atherogenesis?
A
- Proliferate in intima, induced by PDGF, cytokines, NO
* Makes of large part of fatty streak
9
Q
• How do platelets play role in atherosclerosis?
A
- Release factors to promote proliferation of SM
- Part of clotting= yields thrombus
- Extrinsic: activated by blood and vascular elements
- Intrinsic: vascular only (skin, muscle, CT)
10
Q
• What is the fatty streak?
A
- earliest grossly visible pathologic lesion of atherosclerosis
- dt focal accumulation of serum lipoproteins in intima.
- Micro: foam, T, smooth mm cells in varying proportions.
- Seen in aorta and coronary arteries of most individuals by 20 years of age.
11
Q
• What can a fatty streak progress to?
A
- fibrous plaque dt lipid accumulation and migration and proliferation of SM
- SM cells responsible for deposition of ECM CT
- = fibrous cap over foam cells, EC lipid, necrotic cellular debris
12
Q
• Are atherosclerotic plaques random?
A
- lesions of atherosclerosis don’t occur in random fashion.
- Hemodynamic factors interact with the activated vascular endothelium.
- blood shear stresses generated by blood flow modulate genes in endothelium activity of occur in branching, curves, where blood has sudden changes in velocity and direction of flow.
- shear stress and turbulence promotes atherogenesis at important sites in coronary arteries, major branches of TA and AA, large vessels of lower extremities.
13
Q
• What does growth of the fibrous plaque cause?
A
• vascular remodeling, progressive luminal narrowing, blood-flow abnormalities, compromised O2 supply to target organ.
14
Q
• What is ischemia?
A
• imbalance bw supply and demand of blood (O2, nutrients, waste removal) to a tissue
15
Q
• what is Coronary artery disease (CAD)?
A
• describes a reduction in blood flow to cardiac muscle.
16
Q
• What is Ischemic heart disease (IHD)?
A
- Aka: myocardial ischemia
- inadequate supply:demand ratio by heart muscle.
- more a clinical rather than pathological term
- > 90% cases: reduction in coronary blood flow dt atherosclerotic coronary arterial obstruction.
- 10% involves coronary artery spasm or embolism.
17
Q
• What are the 4 major syndromes of clinical manifestation of IHD?
A
- Myocardial infarction (MI): duration/severity causes death of heart muscle.
- Angina pectoris: less severe, doesn’t cause death of cardiac muscle. 3 main types: stable, variant, unstable (may lead to MI)
- Chronic IHD w HF
- Sudden cardiac death.
18
Q
• Is CAD always symptomatic? IHD?
A
- CAD: In most cases, there is a long period (usually decades) of silent, slowly progressive, coronary atherosclerosis before becomes symptomatic.
- IHD: clinical presentations and syndromes are only the late manifestations of coronary atherosclerosis that usually begins during childhood or adolescence.
19
Q
• Why is CAD complex?
A
• dynamic interaction, many processes like fixed atherosclerotic narrowing of coronary arteries, intraluminal thrombosis over disrupted atherosclerotic plaque, resultant platelet aggregation, and vasospasm.
20
Q
• What is the human reaction to plaque formation?
A
- coronary arteries enlarge
* luminal stenosis may only occur once plaque occupies > 40% area bound by internal elastic lamina.
21
Q
• How does lesion progress prior to MI or acute syndromes?
A
- not necessarily a severely stenotic and hemodynamically significant lesion prior to its acute change.
- plaques that undergo abrupt disruption leading to coronary occlusion usu previously produced only mild to moderate luminal stenosis.
- ~2/3 plaques that rupture w total/near-total occlusive thrombosis have < 50% luminal occlusion before rupture
22
Q
• What is the process of a plaque leading up to rupture?
A
- As fibrous cap succumbs to sheer forces or vasospasm, inflammatory cells localize, cause weakening until plaque ruptures.
- Disruption of endothelium exposes thrombogenic contents of core of plaque to circulating blood.
- Rupture of plaque exposes thrombogenic core
- Leads to thrombus formation, partially or completely occlude blood flow
23
Q
• What are the sxs of CAD?
A
- highly variable.
- mild atherosclerosis may have severe angina, MI or sudden cardiac death as their first sx of
- anatomically advanced disease may have few if any sxs, no functional impairment
24
Q
• what are the main sxs of angina and MI?
A
- Chest pain, usu across anterior precordium, tightness, pain, weight
- Pain may radiate to jaw, neck, arms, back, epigastrium.
- Dyspnea indicates poor ventricular compliance w acute ischemia.
25
• What are some additional sxs of angina and MI?
* Diaphoresis
* Anxiety
* Lightheadedness and syncope
* Cough/ wheezing
* N/V or abdominal pain, usu w infarcts of posterior or inferior walls of heart.
26
• What is angina pectoris?
• Paroxysmal usu recurrent attacks of chest discomfort (constricting, squeezing, choking, knifelike) caused by transient (15 sec -15 min) myocardial ischemia wo cellular necrosis of MI
27
• What is stable angina pectoris?
* cardiac ischemia usu dt fixed lesion in coronary artery.
| * Sxs occur only on exertion, generally relieved by rest/medications which dilate arteries, such as nitrates.
28
• What is variant angina?
* Aka Prinzmetal angina.
* exact pathophysiology unknown
* intermittent vasospasm mb key to sx devt
* Pain usu at rest, mmbay be well controlled by vasodilators such as calcium channel blockers.
29
• What is unstable angina pectoris?
* pattern of inc frequency/intensity of chest pain, usu at rest
* prolonged episode may cause MI
30
• what are the ssx of MI?
* PE mb normal, mb asx
* Anxious, agitated, pale, diaphoretic
* HTN- may cause MI, or may be st catecholamines of anxiety and stress
* Hypotension- mb large infarct, often if RV
* Dysrythmias
31
• What are the risks for MI?
* PMHx or FHx of MI (M45
* Younger age, females=outlier, may go undiagnosed
* Cocaine, insulin-dependent, hi cholesterol, FHx CAD
32
• What are the stats on MI deaths?
* >50% occur in pre-hospital setting
* 10% are in-hospital
* 10% of MI occur in first post-infarction year
33
• What are the major types of MI?
* Transmural infarction, usu dt acute coronary thrombosis
* Subendothelial (non-transmural): Coronaries narrowed but patent, Thrombotic occlusion → thrombolysis, short period of ↑ O2 demand/dec O2 delivery
* Hypotension/HTN
* Anemia
34
• What are lab findings with MI?
* ECG may show progression from ischemia to infarction.
* Specific EKG abnormalities can reflect location
* MI dt total coronary occlusion has more homogeneous tissue damage, shown by Q-wave MI pattern on EKG.
35
• How does acute anterolateral MI appear on ECG? Causes? Risks?
* ST elevation in leads over anterior and lateral surfaces
* the more significant the ST elevation , the more severe the infarction.
* loss of general R wave progression across precordial leads
* mb symmetric T wave inversion
* frequently caused by occlusion of proximal left LAD CA, or combined w R CA or LCx.
* Hi risk arrhythmias: LBBB, hemo-blocks, type II second degree AV conduction blocks.
36
• What are the labs reflective of acute MI?
↑ WBC, LDH, cardiac enzymes:
↑ Creatine phosphokinase (MB band )
↑ Troponin (esp. Troponins I and T)
37
• what is CAD?
* Progressive luminal narrowing of CA dt expansion of fibrous plaque, usu dec flow
* >50-70% of lumen diameter is obstructed.
* Sxs: inadequate blood to target organ if inc metabolic activity, or w superimposed coronary spasm
38
• What is AMI?
* myocardial necrosis dt prolonged critical imbalance bw supply and demand of O2 for myocardium
* commonly dt plaque rupture in coronary artery.
* subendothelial area exposed, platelet aggregation, thrombus formation, fibrin accumulation, hemorrhage into plaque, varying degrees of vasospasm.
39
• What are other common causes of AMI?
* Emboli to coronary arteries, mb dt cholesterol or infection.
* Coronary artery vasospasm: if prolonged, w underlying atherosclerotic dz, or poorly functioning heart muscle
40
• What are some additional causes of MI?
* Coronary anomalies: irregular or absent CAs, aneurysms CAs
* Hypoxia dt pulmonary dz, CO poisoning, or other inhaled toxins.
* Arteritis
41
• What is the physiology behind MI?
* Dec O2 to myocardium → anaerobic instead of aerobic metabolism.
* ATP synth dec in 1-2 min; reduced to 50% by 10 mins
* dec ATP disrupts Na+/K+ ATPase = inc membrane permeability of cardiac muscle
* myocytes swell, cellular function declines
* Cal influx activates degradative enzymes, disrupts all cellular function.
* Irreversible cell death in ~15-20 min from onset of injury
* reperfusion in 1-6 hrs may save most of the affected myocardium, dramatic reduction of morbidity and mortality.
* MI may → lethal effects in minutes, aka sudden cardiac death.
42
• What are the gross and histo-pathology changes after MI in the first day?
* 0-0.5 hrs; none; none
* 0.5-4 hrs; none; Glycogen Depletion, seen w PAS Stain and poss. waviness of myocardial fibers at borders
* 4-12 hrs; slight mottling; Initiation of coagulation necrosis, edema, hemorrhage
* 12-24 hrs; dark mottling; Ongoing coagulation necrosis, hypereosinophilia, contraction band necrosis in margins, beginning of neutrophil infiltration
43
• What are the gross and histo-pathology changes after MI at 1-10 days?
* 1-3 d: Infarct center turns yellow-tan; Continued coagulation necrosis, Loss of myocardial cell nuclei and striations, inc neutrophils to interstitium
* 3-7 d: Hyperemia at border with softening yellow-tan center; Begin dead muscle fiber disintegration, neutrophil necrosis, M0 removal of dead cells at border
* 7-10 d: Maximally soft lesion w yellow to red-tan margins; Inc phagocytosis of dead cells at border, begin granulation tissue formation at margins
44
• What are the gross and histo-pathology changes after MI at 10 d- 2 months?
* 10-30 days: Red-gray w depressed borders; Mature granulation tissue w type I collagen
* 2-8 weeks: Gray-white granulation tissue; Inc collagen deposition, dec cellularity
* > 2 months: Completed scarring; Dense collagenous scar formed
45
• What does a 1-day old infarct histo look like?
o coagulative necrosis w wavy fibers (elongated and narrow), compared w adjacent normal fibers (at right). Wide space bw dead fibers contain edema fluid and scattered neutrophils.
o 24 hours post-MI. Note the wavy fibers dt edema. Some viable myocytes present. (left: low mag, right: high mag)
46
• What does 2-day post MI histo look like?
o pt died 2 days post MI, myocytes are irreversibly damaged by loss of nuclei.
47
• What does 7-10 days post MI histo look like?
o Near complete removal of necrotic myocytes by phagocytosis approx
48
• What does 2-month old MI histo look like?
o Well healed myocardial infarct w replaced necrotic fibers by dense collagenous scar. Residual cardiac muscle cells present.
49
• What does gross 6/7/9-day post MI look like?
o 6: sectioned interventricular septum. dead muscle is tan-yellow w surrounding hyperemic border.
o 7: cross section, large anterior LV wall and septum
o 9: Bw 7-10 d, areas of infarction usu have yellow to reddish-tan borders. at autopsy, tissue is pliable and soft to touch.
50
• What does gross 2-month post MI look like?
o previous extensive transmural myocardial infarction of LV. thickness of myocardial wall is normal superiorly, but inferiorly is only a thin fibrous wall.
51
• How long after an MI do cardiac aneurysms most likely occur?
o 2-8 wks, dt formation of thin scar tissue
52
• What are some potential cardiac complications following MI?
o Abnormal LV function ~ proportional to size of infarct.
o Severe "pump failure" (cardiogenic shock), 10-15% post-MI, usu w large infarct (> 40% LV)
o Arrhythmias, usu cause of sudden death;
o Cardiac rupture dt weak, necrotic, inflamed myocardial muscle; hemopericardium and cardiac tamponade usu fatal.
o Hypotension
o CHF
o Hypoxemia
o Pericarditis
o Repeat MI
53
• What is anterior ventricular wall rupture?
o Anterior myocardial rupture 2nd to acute infarction.
54
• What is septal wall rupture?
o Rupture of ventricular septum 2nd to acute MI
55
• What is a hemopericardium?
o Blood trapped in pericardium → hemopericardium. Such a massive amount of hemorrhage can lead to cardiac tamponade.
56
• What is a papillary muscle rupture?
o Complete rupture of necrotic papillary muscle 2nd to acute M.I.
57
• What are potential non-cardiac complications after MI?
o Aspiration
o Infection i.e. pneumonia
o Complications from prolonged immobilization (DVT, PE)
58
• How does pericarditis form after MI?
o Exudative inflammation
o fibrinous or fibrino-hemorrhagic, develops on 2-4th day after transmural MI, dt inflammatory epicardial response to injury
o usu resolves w/o serious consequence or sequelae.
59
• What does fibrino-hemorrhagic pericarditis look like, gross?
o dark, rough epicardial surface over acute infarct.
| o ~17 to 25% of AMI, usu 2-4 days post
60
• What is Dressler's syndrome?
o pericarditis that occurs weeks to months after injury to heart or pericardium.
o Ssx: lo fever, chest pain (usu pleuritic), pericardial friction rub, pericardial effusion.
o AI response to myocardial antigens.
61
• What is optimal blood pressure, by AHA? Pre-HTN? Stage 1 HTN?
o systolic <= 80
o P: 121 -139/ 81 -89
o 1: 140-159/90-99
62
• What are the sxs of HTN?
o Most asx for decades
o 5% have rapid rise in BP, w/o tx mb death in short time (days- 2 yrs)
o > 180-200/> 120 mb severe HA, retinal hemorrhages, papilledema
o Mb dec level consciousness, sz
63
• When is HTN a medical emergency?
o Accelerated, with 1+ sxs
64
• What is primary/essential HTN? Secondary?
o P: 90 -95% has unknown cause
| o S: other 5-10%. many dt chronic renal failure, renal artery stenosis
65
• What causes renal artery stenosis?
o Atherosclerosis primary cause >50; Fibromuscular dysplasia <40
o Other: arteritis, renal artery aneurysm, compression (tumor), neurofibromatosis, fibrous bands
66
• How does renal artery stenosis contribute to HTN? Renal failure?
o macula densa senses dec systemic BP dt reduced blood flow thru narrow artery
o =perceived dec BP, activate RAAS (normally counteracts lo BP)
o Causes HTN (high arterial blood pressure).
o RF: dec GFR, w/o tx
67
• What are some causes of 2nd HTN?
```
o Many
o Drugs, NSAIDs
o Sleep apnea
o Pheochromocytoma
o Hyperaldosteronism (Conn's syndrome)
o Cushing's syndrome
o Hyperparathyroidism
o Acromegaly
o Hyperthyroidism/ Hypothyroidism
```
68
• What are some potential MOA for primary HTN?
o 1) Abn membrane Na transport dt defect/inhibition of Na-K pump
o 2) Inc cellular permeability to Na = inc intracellular Na, cell more sensitive to sympathetic stimulation.
o 3) Ca follows Na, hi intracellular Ca, not Na, responsible for inc sympathetic
69
• What is the purpose of RAAS?
o JGA regulates plasma volume and BP
| o Renin, proteolytic enzyme in granules of the JGA cells, catalyzes angiotensinogen to angiotensin I.
70
• What causes chronic renal dz? What does CRD cause?
o HTN most common, then DM
| o contributes to HTN by incproduction of renin, salt retention, systemic vasoconstriction
71
• What are some complications of HTN?
o leading cause of IHD, PVD, cerebrovascular dz, ventricular hypertrophy, CHF
72
• what risks are reduced with reduced HTN?
o heart attack, CHF, stroke, kidney failure
73
• what are 3 types of HTN?
o labile, benign or accelerated.
74
• What is labile HTN?
o inconsistent BP elevations
o “white coat HTN”: pt get nervous/anxious w dr, hi catecholamines; otherwise normotensive
o Pheochromocytoma: events usu dramatic; paroxysmal HAs, sweats, palpitations, HTN, orthostatic hypotension
75
• What is “benign” HTN?
o very slow development
| o potential sequelae: MI, stroke, RD/RF, PVD, blindness, more
76
• what is an aneurysm?
o “ballooning out” of weak vessel wall, mb dt shear force, hi BP
o Mb any vessel, arteries more common
o Greatest morb/mort: aorta, circle of Willia
o AA: Rupture at 6-7 cm, mb felt as mass in abdomen
77
• What is aortic dissection?
o life threatening complication of hypertension
o blood penetrates intima and enters media layer.
o can affect ascending, aortic arch, descending, and abdominal aorta
78
• What is gross appearance of an aortic dissection?
o red-brown thrombus, intimal tear
o "double lumen" effect
o severe atherosclerosis, cystic medial necrosis, hypertension are risk factors
79
• how does aortic dissection present clinically? Classic aortic arch sx?
o excruciating pain, mb resistant to large doses of morphine
o mb stroke (carotid dissection), MI (coronary dissection)
o if dt HTN, must immediately control BP, to be surgical candidate and inc likelihood of survival
o arch: pain radiating down back, tearing sensation
80
• What is a carotid artery dissection?
o Dissection may occur in carotids
| o Mb caused by aortic dissection ascending to carotid
81
• What is Marfan’s syndrome?
o AD trait; abn CT, dt production of abn fibrillin-1 protein.
o 5–9% of aortic dissections (often fatal)
o Tall, long extremities, digits
82
• How do vessels abnormalities occur in Marfan?
o Aortic aneurysms; usu proximal aortic dissections
| o Weak CT, vessels vulnerable to damage
83
• What are the most serious ssx of Marfan?
o CV: new onset fatigue, SOB, palpitations, tachycardia, new onset murmur
o Mitral/aortic regurgitation
o Often asx, until cystic medial degeneration causes AA/AD (surgical emergency)
84
• How does histology of cystic medial necrosis look?
o mucin stain of aorta wall
| o Pink elastic fibers, instead of running in parallel arrays, are disrupted by pools of blue mucinous ground substance.
85
• Which famous person in hx was thought to have Marfan?
o Abraham Lincoln, but debated
| o more likely had multiple endocrine neoplasia (MEN) type 2B, that caused skeletal features almost identical to Marfan
86
What is CHF?
* heart can’t pump enough blood to get body O2 and nutrients.
* → inadequate emptying of blood at venous side and inadequate blood delivery to both pulmonary and systemic circulation
* =heart failure
87
• What does “left” and “right” circulation refer to?
* Right side has de-oxy blood; lowest P veins entering heart; hi P pulmonic arteries
* Left has oxy-blood; highest P arteries from heart; lo P pulmonic veins
88
• How does heart typically respond to incr demands?
* Inc HR
| * Inc contractility of ventricles
89
• When do signs of CHF begin?
• As demands on heart outstrip normal range of physiologic compensatory mechanisms
90
• What is contractility?
* =inotropic state
* ability of muscle to contract or shorten=myocardial muscle fibers
* stretch in response to inc blood volume during filling of diastole, stretch and shorten when blood is ejected in systole
91
• what happens to contractility of ischemic muscle fibers?
• lose their full elastic recoil forcing healthy muscle fibers to work harder to maintain adequate cardiac output
92
• what happens in acute CHF?
* sympathetic NS and RAAS maintain blood flow and pressure to the vital organs.
* Inc neuro-hormonal activity → inc myocardial contractility, selective peripheral vasoconstriction, salt and fluid retention, BP maintenance.
* Inc fluid retention 2nd by dec hepatic metabolism of aldosterone dt diminished hepatic perfusion 2nd to systemic venous congestion
* causes inc blood volume and venous return (preload) to heart.
* Dec blood to kidneys activates RAAS
* causes renal arteriolar constriction, dec GFR, inc reabsorption of sodium from proximal and distal tubules.
* Result is inc fluid retention
93
• What happens in chronic CHF?
myocardial cells eventually die → necrosis (or from apoptosis) → fibroblast proliferation, scarring → ↑ ventricular wall thickness, CHF worsens → blood/fluid stasis in lungs → heart failure cells
94
• What is the cycle of chronic CHF?
Heart damage → ↓CO → ↓renal perfusion → ↑Na retention, ADH, water reapsorption → fluid overload/edema → heart damage, etc
95
• What are heart failure cells?
• hemosiderin containing macrophages in alveoli
96
• what primary heart dos may result in CHF?
• CAD, valvular dos, cardiomyopathies
97
• What are precipitating factors of CHF?
* Asx: ssx dt unrelated illness or stress
* Common: cessation of cardiac drugs, like a diuretic
* Cardiac pts usu on many drugs, may stop 1 bc: money, poor compliance, side effects, perception of diminished need for medication.
* Ex: cessation of diuretic, but requires for volume optimization. May → Na and water retention and worse CHF
* Dysrythmias a
* Tachycardia: cause dec diastolic filling time , → dec SV
* Tachycardia may cause angina dt inc myocardial O2 demand
98
• What cardiac conditions is cardiac failure most common?
• that result in dec contractility
99
• what are common underlying conditions that can cause impaired myocardial muscle fxn? Systemic that cause CHF?
* inflammatory or degenerative muscle dzs of heart, atherosclerosis, HTN, myocardial ischemia, infarction
* Systemic: Inc BMR (fever), Anemia/hypoxia dec O2 supply, resp/metabolic acidosis/ electrolyte imbalances (hypocalcemia) dec myocardial contractility → dec CO
100
• How is CHF classified?
* Acute vs. chronic
* Right vs. left
* Compensated vs. decompensated
* Low output vs. high output
101
• What happens w LCHF?
* LV can’t produce adequate SV to overcome resistance → dec CO
* can → pulmonary congestion dt inc LV end-diastolic P and inc LA
* usu dt LV infarction, HTN, mitral valve dz
* Blood overfills ventricle dt damaged heart muscle, overflows back into lungs causing pulmonary complications
102
• What causes LCHF?
* IHD
* HTN
* Aortic and mitral valvular dz
* Non-ischemic myocardial dzs
103
• What is RCHF? Causes?
* Dt ineffective RV contraction
* most common cause: LCHF
* Isolated RCHF uncommon
* Acute conditions such as RV infarction or PE can cause isolated RCHF
104
• What is cor pulmonale? Cause?
* Enlarged RV causs heart failure
| * directly dt pulmonary disease: emphysema, chronic bronchitis, PE, PH
105
• what causes pulm htn? And cor pulmonale?
* most commonly dt COPD (emphysema, chronic bronchitis)
| * Any dz that causes chronically low blood O2 may lead to PH and CP
106
• What are ssx of L/R CHF?
* Classic: Fatigue, coughing, edema, weight gain
* Pure LCHF: signs of pulmonary venous congestion
* pure right: signs of systemic venous congestion.
* Both L and R can affect the other → combo of both S and P
* Cough dt fluid in lungs (pulm edema), worse lying
* Easy exhaustion (not enough blood/O2 to heart)
* Edema: feet, ankles, legs, belly (fluid backs up from weak heart)= rapid weight gain
107
• What is the so-called nutmeg liver?
• Gross appearance of liver congestion dt CHF
108
• What is micro histo appearance of liver congestion dt CHF?
• Micrograph of congestive liver demonstrating perisinusoidal fibrosis and centrilobular sinusoidal dilation.
109
• What are high and lo output failure? Sxs?
* Another type of CHF
* Like pump that is either working too heart or not enough → ineffective
* High: peripheral vasodilatation and warm extremities
* Low: vasoconstriction and cool
110
• What causes HO CHF?
* Hyperthyroidism
* Stimulants: cocaine, meth
* Anemia: lo O2 carrying capacity, inc HR → failure
* Paget’s dz: abn bone growth dt inc osteoblast activity → vascularity, needs more blood
111
• What causes LO CHF?
* heart contractibility has weakened: MI, ischemia → ventricular dilation or hypertrophy
* infections: endocarditis, myocarditis
* often seen in late stage CHF
