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Patho > Patho Exam 3 > Flashcards

Patho Exam 3 Flashcards

1
Q

cardiac specific protein not normally found in serum, released only when myocardial cell death has occurred

A

troponin

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2
Q

reflects ventricular contraction, the cardiac work phase

A

systolic

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3
Q

infection of the cardiac endothelium that most commonly affects the heart valves

A

endocarditis

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4
Q

non-st segment elevation myocardial infarction; occurs when damage is not completely through the heart well, heart attack does not go through the myocardium

A

NSTEMI

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5
Q

classification of MI based on ECG; ST segment elevation myocardial infarction; occurs because oxygen needs of the myocardium are not met

A

STEMI

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6
Q

also known as electrical cardioversion, electrical shock that can restore a normal heat rhythm in cardiac arrest or ventricular arrhythmia

A

defibrillation

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7
Q

durable blood clot

A

thrombus

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8
Q

enzyme whose function is to regulate BP and filtration rate of the glomerulus

A

renin

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9
Q

to choke: chronic chest pain that the pt has experienced in the past & feels similar to past episodes

A

stable angina

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10
Q

a cardiac isoenzyme released & increased from dead myocardial cells

A

CPK-MB (creatine phosphokinase muscle/brain

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11
Q

death of tissue as a consequence of prolonged ischemia

A

infarction

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12
Q

chronic inflammatory disease affecting the arterial wall that’s caused by agents that damage the endothelial cells

Plaque build up on arterial wall

this is a common type of arteriosclerosis that develops from plaque buildup

A

atherosclerosis

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13
Q

inadequate blood flow

A

ischemia

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14
Q

the heart’s pumping action is restricted because of an accumulation of fluid surrounding it

A

tamponade

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15
Q

pacemaker other than SA or AV node is initiating a contraction: ventricles are beating independently

A

premature ventricular contractions (PVCs)

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16
Q

smooth, contagious surface of cells that blanket all the inner linings of the arteries

A

endothelium

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17
Q

absence of coordinated, rhythmic atrial contractions: rate & rhythm are irregular… this is the most common arrhythmia and can cause thrombus formation so increased risk of stroke

A

AFIB (atrial fibrillation)

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18
Q

immediate treatment needed for MI: morphine (pain), oxygen (O2), nitrates (vasodilation to increase blood flow to the myocardium, aspirin aka anti-platelet)

A

MONA

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19
Q

reflects ventricular relaxation, cardiac rest phase

A

diastolic

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20
Q

chest pain occurring for the first time or is unlike prior episodes; not relieved by rest

A

unstable angina

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21
Q

decrease in BP that occurs when changing position from lying to standing, this causes a decrease in cerebral perfusion that leads to dizziness

*often experienced by elderly and ppl on antihypertensive meds

A

orthostatic HTN

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22
Q

what does orthostatic HTN cause? what are the s/s?

A

causes a temporary internal of inadequate cerebral perfusion

s/s: fainting (syncope), dizzy, weak, tachycardia, diaphoresis

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23
Q

Type of MI when the artery is completely occluded, completely through the heart wall.

*There are also calls ECG changes during this such as T-wave inversion, ST-segment elevation, Q wave development

A

STEMI (ST Elevation Myocardial Infarction)

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24
Q

Type of MI where the artery is partially occluded causing a milder infarction, subendocardial and not completely thought the heart wall

A

NSTEMI (Non-ST Elevation Myocardial Infarction)

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25
Q

What causes an acute MI occur?

A

a coronary artery is completely obstructed by atherosclerotic plaque or clot, & blood flow carrying oxygen to the myocardium is blocked

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26
Q

this is a dead area of the cardiac muscle that is not perfused with coronary artery blood flow

A

MI

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27
Q

s/s of acute MI aka acute coronary syndrome (ACS)

A

-diaphoresis
-dyspnea
-extreme anxiety
-Levine’s sign (fist to chest)
-pallor
-crushing chest pain that radiates to shoulder, left arm, jaw or back
-weak pulses

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28
Q

diagnostic tests for an MI

A

-ECG
-Serum cholesterol, LDL, HDL
-serum electrolytes
-serum glucose
-hs-CRP
-serum homocysteine
-cardiac enzymes: CPK-MB
-cardiac troponin (cTn)
-CT scan
-cardiac Cath

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29
Q

this is when chest pain occurs for the first time

A

unstable angina

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30
Q

this is chronic chest pain, the pt has experienced in the past and feels similar to past episodes, triggered by physical activity and caused by transient myocardial ischemia

also called chronic coronary artery disease

A

stable angina

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31
Q

this is a squeezing pain in the chest that occurs when there is a lack of blood flow to the myocardium

A

angina

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32
Q

what is the treatment for chronic stable angina?

A

-nitroglycerin preparations
-sublingual glyceryl trinitrate tablets
-NTG spray (glyceryl trinitrate spray)
-nicorandil (K+ channel activator)
-ranolazine (inhibits the late Na+ current, improves myocardial relaxation)
-ivabradine (reduces firing rate of SA node)
-long acting nitrates such as oral isosorbide mononitrate (this can cause headaches, hypotension, lightheadedness)
-transdermal patches

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33
Q

what is an acute MI aka acute coronary syndrome (ACS)

A

occurs when the heart tissue endures prolonged ischemia without recovery

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34
Q

a less-than-normal amount of blood flow to part of your body which means your tissues aren’t getting the oxygen they need

A

ischemia

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35
Q

the gradual process by which plaque builds up on the body’s arterial walls.
This is a chronic, progressive disease w/ a long asymptomatic phases.

A

atherosclerosis

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36
Q

what are risk factors for atherosclerosis (modifiable vs non modifiable)

A

non-modifiable:
-gender: males
-age: over 45 for males, over 55 for females
-race: AA
-family hx: hypercholesterolemia, DM, MI, HTN, stroke

modifiable: high fat & high sodium diet, physical inactivity aka sedentary lifestyle, obesity, high triglycerides over 150 mg/dl, high stress, diabetes, hypertension, alcohol & tobacco use

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37
Q

this is when a pt has chest pain at rest, caused by coronary artery vasospasm, can be associated w/ MI, life threatening ventricular arrhythmias, sudden death

A

prinzmetal’s angina aka vasospastic angina

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38
Q

risk factors for prinzmetal’s angina (vasospastic angina)

A

risk factors have no directly been associated w/ this except:
-cigarette smoking
-inflammatory states, as evidenced by high levels of hs-CRP
-drugs
-cold water can cause spasms in the coronaries as well as valsalva maneuver, hyperventilation, & coronary manipulation

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39
Q

how to treat prinzmetal’s angina (vasospastic angina)

A

-IV or sublingual NTG and calcium blocker antagonist (first line treatment)
-long acting nitrates

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39
Q

how to diagnose prinzmetal’s angina (vasospastic angina)

A

-cardiac monitoring for 24-48 hrs
-coronary angiography
-serial cardiac enzyme assays
-ECG may show ST-segment elevation or depression

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40
Q

risk factors for stable angina aka chronic coronary artery disease

A

same as Atherosclerosis risk factors:
-high cholesterol / triglyceride levels
-high blood pressure
-smoking
-diabetes
-obesity
-physical activity
-eating saturated fats.

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41
Q

this is the hardening & narrowing of the arteries, plaque builds on the arterial walls & restricts blood flow

A

arteriosclerosis

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42
Q

what should not be administered with sildenafil (viagra)? & why?

A

NTG (nitroglycerin) and other nitrate preparations bc it can cause severe hypotension

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43
Q

if a pt takes 3 NTG tablets within 15 mins and no relief of chest pain, what do we assume?

A

the pt is having an MI

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44
Q

what is treatment for unstable angina?

A

we want to prevent MI, so educate!
-antihypertensive, antilipidemic, or anti diabetic meds
-morphine, oxygen if under 95%, nitrates (vasodilators), aspirin

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45
Q

risk factors for unstable angina

A

same as those w/ arteriosclerosis:

-cigarette smoking
-DM
-hypercholesterolemia
-systemic hypertension
-LV hypertrophy
-obesity
-elevated serum levels of homocysteine, triglycerides, LDLs
-low levels of HDLs

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46
Q

how to diagnose unstable angina?

A

very similar to arteriosclerosis diagnose
-bp measurement
-total blood cholesterol
-LDL, HDL, triglycerides measurements
-ECGs
-high sensitivity C-reactive protein (CRP)
-high sensitivity cardiac troponin (hs-cTn)
-chest x ray or CT scan

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47
Q

what is RAAS? & how does it work

A

-Renin-angiotensin-aldosterone system (RAAS) is a key part of BP regulation

-RAAS is a multistep reaction that raises bp in response to diminished circulation in the body.

It works by:
-when bp is diminished, the kidney is sensitive to the drop in bp so renin (enzyme released by juxtaglomerular apparatus of nephrons in response to decreased perfusion) is released into blood stream stimulating the liver to release large protein aka angiotensinogen.

-In the lungs, angiotensinogen is transformed into angiotensin I then angiotensin converting enzyme (ACE) changes angiotensin I into angiotensin II which is an arterial vasoconstrictor which stimulates the adrenal gland (and raises bp) to release the hormone aldosterone.

-aldosterone works at the nephron to increase Na & H2O reabsorption into bloodstream & secrete potassium into nephron tubules. Retention of Na & H2O increases volume of bloodstream and bp!

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48
Q

how does atherosclerosis work? (Patho)

A

-begins after endothelial injury
-WBCs & platelets are drawn to injury
-WBCs engulf & digest LDL
-forms the foundation for arteriosclerotic plaque (makes narrowed artery)

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49
Q

low density lipoprotein, deposited on artery walls

what level should it be?

A

LDL (lousy!!!!!)

less than 130

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50
Q

high density lipoprotein, type of cholesterol that is excreted

**cardioprotective because it carries cholesterol away from the artery walls to be excreted

What level should it be?

A

greater than 60

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51
Q

what are the 2 types of hypertensions?

A

primary- aka essential hypertension, has no known cause

secondary- occurs due to a disease or condition that is known (ex: kidney disease, hormone disorders, oral contraceptives, some drugs

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52
Q

risk factors for hypertension

A

-age
-gender (males)
-AA
-family hx
-obesity
-insulin resistance
-increased salt intake
-alcohol
-diabetes
-tobacco
-sedentary behavior
insufficient vit D & potassium

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53
Q

what are the stages of high blood pressure?

A

-Elevated: 120-129 / less than 80
-Stage 1: 130 - 139 / 80 - 89
-Stage 2: 140 - 179 / 90 - 119
-Hypertensive crisis: 180+ / 120+

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54
Q

treatment of hypertension

A

major lifestyle changes:
-decreasing salt/sugar intake
-stop smoking and drinking alcohol
-lose weight

or medication therapy

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55
Q

complications of hypertension

A

-heart failure (initially form increased after load from increased peripheral vascular resistance in arterioles)

-atherosclerosis (from damage to blood vessels)

-MI or stroke

-damage to blood vessels which can affect eyes, kidneys, & increase risk for aneurysms

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56
Q

this lab is elevated during acute heart failure

A

BNP (B-type natriuretic peptide)

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57
Q

unilateral leg pain, edema, erythema, warmth

A

DVT

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58
Q

heart attack from a partially occluded artery

A

NSTEMI

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59
Q

SBP between 120 - 129mmHg and DBP < 80 mmHg

A

elevated blood pressure

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60
Q

risk factors for varicose veins

A

-sedentary lifestyle
-pregnancy
-increased age
-female
-leg crossing
-obesity
-prolonged sitting or standing

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61
Q

this causes back flow from one chamber to another

A

regurgitation

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62
Q

pts w/ hepatic encephalopathy (change in mental status/confusion) will exhibit elevated levels for this lab

A

ammonia

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63
Q

this is the pacemaker of the heart

A

SA node

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64
Q

this lab indicates death to myocardial muscle cells

A

troponin level

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65
Q

most common risk factor for diverticulosis

A

low fiber diet

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66
Q

one cause of HF due to uncontrolled hypertension causing an enlarged and weakened heart

A

LVH (left ventricular hypertrophy)

**systolic = life sided HF

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67
Q

reduction in blood flow to tissue

A

ischemia

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68
Q

this causes RUQ pain after eating fatty meal, stone in common bile duct, four Fs

A

cholecystitis

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69
Q

this causes narrowing of a heart valve, obstructing forward blood flow

A

stenosis

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70
Q

death of tissue d/t obstructed blood supply

A

infarction

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71
Q

heart attack from a totally occluded artery

A

STEMI

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72
Q

these labs will be elevated in pts w/ acute pancreatitis

A

amylase & lipase

***Increased serum lactic dehydrogenase & C-reactive protein are indicative of severe panc

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73
Q

pericardial sac fills w/ fluid and compresses the heart

A

tamponade which causes reduction in SV & CO which will drop bp.. this causes HR to increase in order to overcome the low bp

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74
Q

common sign of diverticulitis

A

LLQ pain

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75
Q

risk factor for esophageal cancer

A

GERD

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76
Q

what is portal HTN and who does it occur in

A

increased pressure within the portal venous system

occurs in alcoholics, pt w/ cirrhosis & ascites

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77
Q

SBP greater or equal to 140
DBP greater or equal to 90

A

stage 2 HTN

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78
Q

dyspnea and cough is a s/s of what type of heart failure

A

LV failure

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79
Q

rhythm disorder in which ventricles beating independently without signal from SA or AV node

aka extra heartbeats

A

PVCs (Premature ventricular contractions)

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80
Q

pain in BLE w/ activity that improves with rest

A

intermittent claudication

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81
Q

what is volvulus

A

twisting of the intestine

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82
Q

this conduction disorder shows irregular rhythm w/ loss of atrial kick

A

Afib (atrial fibrillation)

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83
Q

common s/s of celiac disease

A

diarrhea, abdominal pain, weight loss

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84
Q

an ejection fraction of what % is indicative of HF?

A

less than 40%

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85
Q

what are the 3 layers of an arterial wall

A
  1. tunica adventitia (connective tissue, outer layer)
  2. tunica media (smooth muscle, middle layer, expands to accommodate pressure)
  3. tunica intima (interior lining of artery made of basement membrane & endothelial cells)
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86
Q

this is responsible for growth of new blood vessels (angiogenesis),

collateral branches of arterioles form in response to this

A

VEGF (vascular endothelial growth factor)

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87
Q

when blood is excessive, this types of cells produce C-natriuretic peptide to promote diuresis (reduces bp)

A

endothelial cells

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88
Q

this causes vessel constriction which raises bp

A

endothelin

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89
Q

what is prostacyclin vs thromboxane A2

A

prostacyclin = clot formation
thromboxane A2 = clot prevention

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90
Q

this causes vessel dilation (opens vessels, improves blood flow, lowers bp)

A

nitric oxide

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91
Q

this activates clotting

A

von Willebrand factor

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92
Q

laminar vs turbulent blood flow

A

laminar = smooth flow parallel to vessel

turbulent = rough flow perpendicular to vessel

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93
Q

cardiac contraction (s or d)

A

systole

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94
Q

cardiac relaxation (s or d)

A

diastole

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95
Q

amt of blood ejected per beat

A

stroke volume

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96
Q

this is the amt of blood pumped by LV per minute
HR x SV

A

cardiac output

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97
Q

what is FH? & what are risk factors

A

familial hypercholesterolemia which is a specific type of hyperlipidemia

risk factors - FH, DM, obesity, hypothyroidism, lack of physical activity, some meds

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98
Q

s/s of hypertension

A

-often no signs
-organ sign damage: headaches, chest pain, vision disturbances, dizziness
-protein in urine, LVH on ECG, bruits bc turbulent flow, alteration in PMI, retinal vessels

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99
Q

s/s of atherosclerosis

A

only symptom is weak pulse and bruits

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100
Q

how to diagnose PAD (Peripheral Arterial Disease)

A

-ankle-brachial index (Ratio of the BP in lower legs to arms)
-CBC
-lipid profile
-inflammatory markers
-impedance arterial
-CT
-coventional angiography
-MAR (magnetic resonance angiogram)
-duplex & plethysmography ultrasonography

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101
Q

treatment of PAD (peripheral arterial disease)

A

-lifestyle modification (exercise)
-meds (cholesterol lowering, anti hypertensive, platelet inhibitors, vasodilators, thrombolytic agents (prevents DVT or PE bc high risk of blood clot)

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102
Q

arterial dysfunction & reduced blood flow within the lower extremities, most common site is femoral artery above knee… gradual onset

-pulse is not palpable in this lower extremity

A

peripheral arterial disease (PAD)

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103
Q

Weakened segment of the artery that creates an outpouching that is susceptible to rupture & can cause turbulent blood flow within the artery which causes bulging of walls or dilation (enlarging of the walls)

A

aneurysm

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104
Q

largest blood vessel in body

A

aorta

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105
Q

who is at risk for aneurysm

A

smokers

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106
Q

a true one of these involves all three layers of vessel wall

A

true aneurysm

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107
Q

these are classified by size, shape, location

A

aneurysm

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108
Q

what is a false aneurysm

A

hematoma where the clot is outside arterial wall

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109
Q

weakness on one side of vessel (aneurysm)

A

saccular shape

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110
Q

all layers of vessel wall dilate equally (aneurysm)

A

fusiform shape

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111
Q

s/s of aneurysm

A

n/v in AAA

no signs if cerebral aneurysm

112
Q

treatment of aneurysm

A

-stop smoking
-regulate BP
-surgical treatment
-FU yearly or every 6 months

113
Q

sudden severe headache then mental status change

A

subarachnoid hemorrhage (aneurysm)

114
Q

acute coronary syndrome (ACS) vs. myocardial infarction (MI)

A

ACS- due to ischemia

MI- due to prolonged ischemia leading to cell death

115
Q

3 layers of heart wall

A

-epicardium (outer)
-myocardium (muscle, middle)
-endocardium (interior)

116
Q

classic ECG changes with MI

A

-T wave inversion
-ST Segment elevation
-Q wave development

117
Q

biochemical markers w/ MI

A

-elevation of Troponin & T
-increase in CPK-MB (creatinine phosphokinase)

118
Q

this is a surgical option for angina, this creates new routes around occlusions (makes new vessels to bypass the ones that are no longer functioning)

A

CABG (coronary artery bypass graft)

119
Q

what does a ST-segment elevation on a EKG show?

A

MI

120
Q

myalgia vs arthralgia

A

myalgia = muscles aches/pain
arthralgia = joint pain

121
Q

s/s of Vfib (ventricular fibrillation)

A

loss of consciousness , death may occur because this is life threatening!

122
Q

contraction is uncoordinated with no effective pumping during this. you have to shock pt to reset the heart if this occurs

A

Vfib (ventricular fibrillation)

123
Q

in HF, this is decreased d/t weak LV that cannot adequately pump blood out of chamber

A

CO (cardiac output)

124
Q

amt of blood in heart at end of diastole, causes stretch & increased pressure in ventricular chamber increasing SV

A

preload

125
Q

amt of resistance the ventricle overcomes to pump blood out of heart

increased this reduces cardiac output

A

afterload

126
Q

this is the volume of blood pumped w/ each ventricular contraction

this should be 60-70% in healthy ppl, if under 40% then HF!

A

LVEF (left ventricular ejection fraction)

127
Q

4 changes that contribute to development of heart failure

A
  1. increased fluid volume
  2. impaired ventricular filling
  3. degeneration of ventricular muscle
  4. decreased ventricular contractile function
128
Q

cor pulmonale (an enlarged right ventricle in your heart that happens because of a lung condition

A

right sided heart failure

129
Q

risk factors for HF

A

age
AA
DM
lifestyle- obesity, tobacco, alcohol, sedentary lifestyle
family hx
breathing issues
heart disorders
kidney conditions
meds: antifungals, anabolic steroids, chemotherapeutic angets

130
Q

types of HF

A
  1. left ventricular HF:
    -systolic, decreased contractility so weak floppy heart
    -diastolic HF so decreased relaxation due to thick ventricles
    -PND (paroxysmal nocturnal dyspnea) aka fluid accumulates in lungs while supine
  2. right ventricular HF:
    -weak RV, causes backup of blood into right heart chambers
    -causes organomegaly, ascites, hypoxia
  3. high output HF:
    -uncommon cause, severe anemia
131
Q

LVF vs RVF (right ventricular failure)

A

LVF: affects breathing (dyspnea, cough, orthopnea, PND, weak pulse, decreased cerebral perfusion)

RVF: affects gut (JVD, ascites, GI disturbances, hepatomegaly, splenomegaly, peripheral edema, hepatojugular reflex)

132
Q

how to diagnose HF

A

-elevated BNP (greater than 100pg/ml)
-diluted electrolytes due to fluid retention
-chest x ray (cardiomegaly, vascular congestion in pulmonary fields)
-ECG (no specific sign, but may see elevation of ST segment)
-Echo (estimates LVEF)
-MGAS (multiple gate acquisition scan)
-cardiac Cath
-angiography (use of dye to view vessels)

133
Q

how to treat HF

A

-diuretics (to reduce fluid vol)

-aldosterone antagonist (reduce fluid vol)

-ACE inhibitors (blocks angiotensin converting enzyme)

-angiotensin II receptor blockers (ARBs for those who can’t tolerate ACE inhibitors and good for diabetics bc protects renal)

-Beta 1 adrenergic blockers (slows HR, lessen vasoconstriction)

-positive inotropic & negative chronotropic agents (increases force & HR)

-synthetic natriuretic

-nitrates

-arterial vasodilators

-neprilysin inhibitors (breakdowns BNP and ANP)

134
Q

this might develop in HF due to constant aldosterone

A

hypokalemia (low K)

135
Q

this is severe RVF which leads to massive peripheral edema, affects most of tissues of body

A

anasarca

136
Q

if this is elevated, then indicative of HF

A

BNP

137
Q

adverse effects of this is hyperkalemia, angioedema, cough … this treats HF

A

ACE inhibitors

138
Q

this has negative side effects that require careful monitoring, med for HF

A

inotropic drugs

139
Q

these have a hypotensive effect if combined w/ sildenafil meds

A

nitrates

140
Q

must take apical pulse for 1 full minute w this medication that helps HF, it can slow the HR excessively

A

digitalis

141
Q

this is the mitral and tricuspid valve closure (atrioventricular valves), known as S1 aka the lub

A

Systole

142
Q

this is the aortic & pulmonic valve closure (closing of semilunar valves), known as S2 aka the dub

A

diastole

143
Q

S3 vs S4

A

S3 = kentucky
S4 = Tennessee

144
Q

when you have this, you are at risk for LVH

A

stenosis

145
Q

narrow opening which is high resistance to flow, excess blood is left behind, can increase workload on heart

A

stenosis

146
Q

when you’ll hear murmurs

A

MSARD (mitral, stenosis, aortic, regurgitation, diastole)

MRPASS (mitral, regurgitation, pulmonary, artery, stenosis, systole)

MVP (mitral valve prolapse)

147
Q

this is when narrow mitral valve hinders blood flow into the left ventricle, so blood flow backs up in the left atrium causing enlargement, pressure builds backward into pulm veins which causes pulmonary edema

one of the most common heart valve disorder!

A

mitral stenosis

148
Q

how to grade murmurs? when is it dangerous?

A

grade 0-6
0 = no murmur, 6 = so loud
3-6 is dangerous

149
Q

s/s of mitral stenosis

A

dyspnea w/ exertion, PND (paroxysmal nocturnal dyspnea), orthopnea

150
Q

this is also known as regurgitation

A

mitral valve insufficiency which increases risk of HF & death … MV fails to close, allowing back flow of blood into LA as LV contracts

151
Q

s/s of mitral insufficiency aka regurgitation

A

-chest pain (decreased coronary flow)
-pulmonary symptoms due to fluid backup in lungs
-Afib
-diminished S1 sound bc leaflets don’t close

152
Q

this is intermittent episodes of mild mitral insufficiency, often asymptomatic, can be part of Barlow’s disease aka floppy heart valve syndrome

A

MVP (mitral valve prolapse)

153
Q

this is a common cause of mitral insufficiency, affects females 14-30, common in ppl w/ genetic connective tissues disorders such as Marfan’s, osteogenesis imperfect, ehlers-danlos syndrome but in most cases is unknown
; commonly asymptomatic , SYSTOLIC heart murmur

A

MVP (mitral valve prolapse)

154
Q

this is the calcification of the aortic valve, it’s difficult for LV to pump blow which increases resistance, LVH

A

aortic stenosis (AS)

155
Q

s/s of aortic stenosis (AS)

A

-exertion dyspnea
-pulmonary edema
-angina pectoris
-carotid arterial pulse rises slowly w/ a delayed peak
-lateral displacement LV impulse
-murmur is systolic, crescendo & low pitched

156
Q

this is a genetic disorder that inhibits ejection of blood from LV, diamond shaped systolic murmur, leading cause of sudden death in young

A

(HCM) hypertrophic cardiomyopathy

157
Q

this is due to incomplete closure of AV, allows. backward leakage of blood into LV during diastole
-Austin flint murmur

A

aortic insufficiency
-can be acute or chronic, more common in men / peaks at 40-60 of age

158
Q

3 different types of venous disorders

A
  1. DVT
  2. PE
  3. VTE
159
Q

these return deoxygenated blood to heart and have a low type of pressure

A

veins

160
Q

this occurs b/c of poor venous return, associated with immobility, sedentary behavior or valve dysfunction within the leg veins.

A

venous stasis

161
Q

D-dimer test is used to diagnose this, if positive (over 500)

A

DVT

162
Q

why is pancreatitis dangerous?

A

because chronic inflammation can lead to fibrosis, strictures, and cyst formation

163
Q

s/s of pancreatitis

A

-Pain, sometimes very severe (main manifestation)
-Fever
-Nausea
-Vomiting
-Leukocytosis

164
Q

what it the most common cause of chronic pancreatitis

A

chronic alcohol abuse.

165
Q

____________ is a stable virus spread by blood products, bodily fluids, or sexual contact

what are s/s

A

Hep B

▪ Fatigue
▪ Vomiting
▪ Anorexia
▪ Malaise
▪ Abdominal pain ▪ Fever
▪ Myalgias ▪ Headache
▪ Jaundice
▪ Dark urine
▪ Light-colored stools o Risk Factors
▪ Non-Hispanic black ethnicity
▪ Cocaine use
▪ High number of sexual partners
▪ Unprotected sex
▪ Sexually transmitted
infection
▪ Human
immunodeficiency virus
▪ Handling blood products
▪ Intravenous drug use
Male homosexuality
▪ Hemodialysis
▪ Living with someone with HBV

166
Q

______ is transmitted via blood as in intravenous drug use, sexual transmission is not as likely

what are the s/s

A

Hep C

▪ Fever
▪ Vomiting
▪ Anorexia
▪ Malaise
▪ Abdominal pain
▪ Myalgias
▪ Headache
▪ Jaundice
▪ Dark urine
▪ Light colored stools
Risk Factors- High IV drug use, Cocaine with shared straws

167
Q

____ is transmitted via ingestion of contaminated food/water or contracted by unsanitary conditions from person-to-person

what are the S&S

A

Hep A

▪ Flu-like symptoms
▪ Hepatomegaly
▪ Jaundi
Pale stools
▪ Dark urine
▪ Pruritus

Risk factors:
▪ Weak immune system, Living in unsanitary conditions, Institutionalization, Foreign travel to a country where HAC is endemic, Male homosexuality, Illicit parenteral drug use

168
Q

This is aged RBC or Hgb. Conjugated in liver and put in bile. Starts unconjugated (increases with dysfunction) and becomes conjugated- stored in bile (water soluble- excreted).

A

bilirubin

169
Q

what causes endocarditis?

A

mainly bacteria, but fungal can too

170
Q

how to diagnose endocarditis

A

based on a set of specific clinical signs as well as labs and echocardiographic findings called DUKE criteria (1 major findings 3 minor findings OR 5 minor findings)

171
Q

treatment of endocarditis

A

mainly IV antibiotics for 6 weeks or longer or high dose oral antibiotics

172
Q

who is at risk for endocarditis

A

pts w/ underlying valvular heart dz & those who illicit IV drugs

can also be over 50 or hospital acquired infection

173
Q

this is caused by fluid accumulation in the lungs

A

PND (paroxysmal nocturnal dyspnea)
this is sudden SOB that occurs in middle of night

174
Q

this is caused by fluid accumulating in the pulmonary interstitial spaces

A

orthopnea

175
Q

how to treat inflammation of the esophagus

A

-Proton pump inhibitor (PPI)
-Histamine-2 blocker (H2 blocker)

176
Q

most common cause of GERD (Gastroesophageal Reflux Disease)

A

functional or mechanical problem that decreases muscles tone of the LES (lower esophageal sphincter), which allows for regurgitation of stomach contents into the esophagus

177
Q

s/s of GERD (Gastroesophageal Reflux Disease)

A

Dysphagia
Heartburn
Epigastric pain
Regurgitation
Dyspepsia (indigestion)
Acid indigestion

178
Q

treatment for GERD (Gastroesophageal Reflux Disease)

A

-PPIs (proton pump inhibitors) Most effective! OTC or Rx
-H2RAs (histamine-2 receptor antagonist)
-lifestyle changes
-transoral inåisionless fundoplication (TIF)
-laparoscopic antireflux (fundoplication)

179
Q

What condition is considered to be pre-cancerous and requires frequent evaluation?

A

Barrett’s Esophagus which results from GERD

180
Q

what does stool w/ melena look like? (s/s of chronic upper gastrointestinal bleed)

A

black & tarry

181
Q

what is hematemesis, common in upper GI bleeds

A

vomit w/ bright red blood & “coffee grounds” which indicates the blood has mixed with the acid of the stomach

182
Q

This is engorged esophageal veins,
Often due to portal vein hypertension or Liver issue (Jaundice may be present)
***Veins may rupture

A

Esophageal Varices

183
Q

risk factors for GERD (Gastroesophageal Reflux Disease)

A

obesity
smoking
age
sedimentary lifestyle
anxiety/depression

184
Q

Stomach pushes up through opening in diaphragm

A

hiatal hernia (upper stomach)

185
Q

how to diagnose hiatal hernia (upper stomach)

A

endoscopy

186
Q

s/s of hiatal hernia (upper stomach)

A

dysphagia
epigastric discomfort
OR may be asymptomatic

187
Q

treatment of hiatal hernia (upper stomach)

A

-surgical repair aka laparoscopic fundoplication

-PPIs (proton pump inhibitors) OTC or Rx

-histamine-2 blockers

188
Q

intestinal protrusion through abdominal wall, more common in males

A

hernia

189
Q

s/s of hernia

A

depends on location/ degree of protrusion

can be asymptomatic or pain near site

*coughing & straining can make it worse

190
Q

most common type of hernia

A

inguinal hernia (inner groin)

191
Q

difference between reducible, incarceration, and strangulation hernia

A

-reducible: returned to normal position with manual pressure

-incarceration: loop of intestine trapped between muscle fibers

-strangulation: blood supply to hernia compromised by pressure

192
Q

diagnose and treatment of hernia

A

diagnose- pt hx & physical exam

treatment- herniorraphy

193
Q

this is known as “sprue” and “gluten-sensitive enteropathy”

condition that occurs form a hypersensitivity reaction to gluten, a by product of wheat, barley, rye

A

celiac disease - autoimmune dz

194
Q

s/s of celiac dz

A

-bloating & diarrhea bc can’t digest carbs
-gas
-steatorrhea (loss of fat in stools)
-malnutrition .. can’t absorb protein or fats so decrease in A (visual disturbances), D, E (RBC damage), K (iron deficiency)

195
Q

how to diagnose celiac disease

A

-serology: celiac panel

-positive antibody titer of IgA anti tissue transglutaminase (IgA TTG)

-intestinal biopsy

196
Q

how to treat celiac disease

A

dietary modificatioon (elimate gluten products)

pt needs vitamin replacement

if extreme, corticosteroids ay be prescribed

197
Q

risk factors for celiac dz

A

-family hx
-DM1
-obesity
-caucasian w/ European ancestors

198
Q

night blindness is associated with what disease

A

celiac dz due to lack of vitamin A

199
Q

what causes SBO?

A

-post op adhesions
-malignancy
-chron’s
-hernia

200
Q

s/s of SBO

A

-varies w/ obstruction severity
-pain
-n/v
-hyperactive bowel sounds
-diarrhea if partial obstruction

201
Q

how to diagnose SBO

A

abdominal X ray

202
Q

how to treat SBO

A

-NG tube (decompress bowel & removes accumulation of fluid)

-meds

-surgery if complete obstruction

203
Q

classic triad for peritonitis (inflammation of peritoneum due to bacterial infection or leakage of intestinal content into peritoneal cavity)

A

abd pain, abd rigidity, rebound tenderness

204
Q

s/s of PE resulting from DVT

A

acute dyspnea (SOB), chest pain, tachycardia (high HR), diaphoresis (sweating), anxiety

205
Q

risk factors for DVT

A

-age
-pregnancy
-birth control
-obesity
-sedentary lifestyle
-smoking
-cancer
-family hx

206
Q

treatment for DVT

A

anticoagulants

207
Q

s/s of IBS (irritable bowel syndrome)

A

-abd pain
-bloating
-distention
-constipation
-diarrhea

208
Q

IBS (irritable bowel syndrome) vs IBD (inflammatory bowel disease)

A

IBS- no pathological changes within interior of bowel

IBD- pathological changes in colon (crohn’s dz, ulcerative colitis)

209
Q

how to diagnose LBO

A

abdominal x-ray

210
Q

how to treat LBO

A

-depends on the cause
-fluid replacement
-intestinal decompression

211
Q

s/s of LBO

A

-abd pain
-abd rigidity
-abd distention
-abd tenderness
-high pitched bowel sounds partial obstruction vs no sounds or feces in complete obstruction

212
Q

SBO vs LBO

A

SBO- n/v
LBO- constipation, abd distention

213
Q

what causes LBO

A

50-60% is caused by cancer of colon or rectum

20% is caused by diverticular disease

5% is caused by volvulus

age, post op, hernia

214
Q

-this is RLQ pain (Mc Burney’s point)
-diagnose this by Psoas sign, Obturator sign
-CT scan is most accurate for diagnosis

A

appendicitis

215
Q

Disorder characterized by abd pain, altered bowel activity in absence of pathology. Also called colitis, irritable colon, spastic colon

A

IBS (irritable bowel syndrome)

216
Q

risk factors for IBS

A

-acute bacterial gastroenteritis
-sedentary work
-lack of exercise
-processed food
-females are 2x more likely
-age
-fam hx
-stress
-possibly hormonal

217
Q

weight loss an iron deficiency anemia are alarming symptoms of this

A

IBS

218
Q

how to treat IBS

A

regulate bowel movements, bulk forming laxatives, antidiarrheals

219
Q

diverticulosis vs diverticulitis

A

diverticulosis: weakened area bowel wall, small outpouchings that collect intestinal contents & form obstruction

diverticulitis: diverticula inflammation

220
Q

risk factor for diverticular disease

A

low fiber diet
age
western culture
genetics

221
Q

s/s of diverticular disease

A

-bowel habits may be altered

-LLQ or RLQ depending on area affected

-depends on severity of inflammation

-fever, tachy, anorexia

222
Q

treatment for diverticular disease

A

diet modification
adequate fluid & fiber intake
or NPO if severe
pain meds

223
Q

what causes volvulus

A

-constipation and high fiber diet
-obstruction & ischemia

224
Q

s/s of volvulus

A

-bilious vomiting
-colicky (aka in waves) & then steady abd pain
-blood, mucus in stool

225
Q

how to diagnose and treat volvulus

A

diagnose w/ upper & lower barium GI series

treatment is surgery

226
Q

high pitched bowel sounds indicate what

A

partial obstruction

227
Q

bowel sounds are absent indicates what

A

complete obstruction

228
Q

what lab shows perforation of the bowel or organ

A

elevated serum amylase

229
Q

what should you do first for acute abdomen pain in females

A

pregnancy test to rule out ectopic pregnancy

230
Q

this can happen in ulcerative colitis or Crohn’s disease, it is a medical emergency

A

toxic megacolon

231
Q

Crohn’s disease vs ulcerative colitis

A

Crohn’s disease: entire GI wall aka transmural (any part of GI), cobblestones, malabsorption

ulcerative colitis: not transmural (only mucosal layer of large intestine), more common, pseudopolyps, precancerous

232
Q

murmur associated with mitral stenosis

A

diastolic, low pitched

233
Q

murmur associated with aortic stenosis

A

systolic, low pitched, crescendo

234
Q

mitral vs aortic stenosis murmur

A

both low pitched, mitral is diastolic whereas aortic is systolic

235
Q

unconjugated vs conjugated bilirubin

A

unconjugated: indirect bilirubin

conjugated bilirubin: direct bilirubin (this is where bilirubin becomes water soluble)

236
Q

bilirubin is derived from what?

A

the breakdown of aged RBCs

237
Q

pts w/ liver dysfunction are at increased risk for what?

A

blood clots!

238
Q

what causes jaundice

A

excessive RBC hemolysis (too much breakdown/destruction), hepatocellular injury, bile duct obstruction

239
Q

this occurs when the liver may not be secreting bile for fat digestion

A

steatorrhea

240
Q

which hepatitis is contaminated food/water and fecal oral

A

Hep A (HAV)

bc A for agriculture aka food
and bc A & E come from the sea aka water
if it ends w/ a vowel then it comes from the bowel!

241
Q

which hepatitis(s) is blood/body fluids

A

Hep B (HBV)
Hep C (HCV)
Hep D (HDV)

242
Q

which hepatitis is contaminated water and fecal/oral route

A

Hep E (HEV)

bc A & E come from the sea aka water.. if it ends w/ a vowel then it comes from the bowel!

243
Q

hepatitis that is blood/body fluids, vertical… rare

A

Hep G (HGV)

244
Q

treatment for varicose veins

A

elevated legs, compression stockings

245
Q

s/s of Hep A

A

fever, abd pain, flu like symptoms

246
Q

s/s of Hep B

A

anorexia
n/v
jaundice
hepatomegaly
fatigue
splenomegaly
flu like symptoms
lymphadenopathy

247
Q

s/s of hep C

A

low grade fever, malaise, n/v, fatigue, jaundice, anorexia, weight loss

248
Q

this disease is silent & gradual, irreversible damage due to collagen & connective tissue infiltration … #1 caused by HCV then alcoholic liver disease, NAFLD

**9th leading cause of death in US

A

cirrhosis

249
Q

s/s of cirrhosis

A

most ppl remain asymptomatic until late stage
-ascites
-hepatic encephalopathy
-variceal bleeding from portal HTN
-peritonitis (inflammation of the peritoneal caused by bacterial infection or leakage of intestinal contents into peritoneal cavity)

250
Q

ppl with this hepatitis can still be carriers of this inactive hepatitis

A

Hep B (HBV)

251
Q

this hepatitis is the #1 cause of cirrhosis

A

Hep C (HCV)

252
Q

risk factors for cirrhosis

A

wide range of diseases and conditions such as:
-chronic alcohol use
-chronic viral hepatitis (B,C,D)
-NAFLD (non alc fatty liver dz)
-CF
-infection such as syphilis
-meds like acetaminophen

253
Q

treatment for cirrhosis

A

nothing except liver transplant if severe

254
Q

this is a serious disorder, potentially lethal but is reversible.

the organ involved gets inflamed and injured due to the leakage of an activated digestive enzyme

A

acute pancreatitis

255
Q

risk factors of acute pancreatitis

A

-biliary dz (cholelithiasis)
-abd trauma
-mumps, varicella, measles, rubella
-hypercalcemia
-hepatits
-excessive alcohol ingestion
-hypertriglyceridemia
-infections
-periampullary tumors
-certain meds

256
Q

s/s of acute pancreatitis

A

-severe abd pain in epigastric region, can radiate to back
-fever
-tachy
-hypotension
-n/v
-diarrhea
-decreased bowel sounds
-jaundice
-abd tenderness, guarding, distention
-cullen sign aka discoloration around umbilicus due to hemorrhage
-grey turner sign aka discoloration around flanks, retroperitoneal bleeding

257
Q

treatment of acute pancreatitis

A

NPO until resolution of pain
fluids for hydration, electrolyte support/balance
low fat diet
pain control

258
Q

s/s of chronic pancreatitis

A

-upper abd pain that radiates to back, worsens w/ eating/drinking and becomes constant, n/v, diarrhea, weight loss, steatorrhea

259
Q

risk factors for chronic pancreatitis

A

-30 to 40y/o
-AA
-alcohol induced in men, lipid induced in women
-genetics if under 30

260
Q

chronic vs acute pancreatitis

A

-chronic does not heal & causes permanent damage .. can happen due to acute pancreatitis

-acute heals and is reversible

261
Q

what labs will be elevated for pancreatitis

A

amylase & lipase !!!

CBC, glucose, CRP as well

262
Q

jaundice may be the first sign of this cancer due to tumor compromising bile duct

A

pancreatic cancer

263
Q

this is the muscle pain that happens when you’re active and stops when you rest.

A

intermittant claudication

264
Q

the resistance in the circulatory system that is used to create blood pressure, the flow of blood and is also a component of cardiac function

A

SVR (systemic vascular resistance) aka Peripheral vascular resistance

265
Q

s/s of PAD (peripheral arterial disease)

A

pulseless
pallor
cold
hairloss
smooth, shiny skin
ulcers

266
Q

2nd leading cause of death resulting from cancer, preventable disease

A

colorectal cancer

267
Q

risk factors for colorectal cancer

A

-males
-age, over 50
-AA
-inflammatory bowel disease (Crohn’s, ulcerative colitis)
-DM
-long term immunosuppression
-high consumption of red meats
-obesity
-tobacco/alc
-low fiber diet, high fat
-sedentary lifestyle

268
Q

s/s of colorectal CA

A

fatigue, weakness, abd cramping, weight loss, iron deficiency anemia, blood in stool, diarrhea, constipation, melena aka dark tarry stools

269
Q

diagnose and treatment for colorectal CA

A

diagnose: colonoscopy, DRE, FOBT, barium enema, abd & pelvic US, CT, MRI, PET scan

treatment: surgical resection of tumor , radiation, chemo, cryotherapy

270
Q

systemic disorder that involves the narrowing of peripheral blood vessels as a result of arteriosclerosis (buildup of plaque), can happen with veins or arteries.

A

Peripheral vascular disease (PVD)

271
Q

narrowing or blockage of your coronary arteries, which supply oxygen-rich blood to your heart. as a result of plaque buildup in these arteries limits how much blood can reach your heart muscle

A

CAD (coronary artery disease)

272
Q

the alternate or “backup” blood vessels in your body that can take over when another artery or vein becomes blocked or damaged.

A

collateral circulation

273
Q

the measurement of the percentage of blood leaving the heart each time it squeezes

A

ejection fraction
normal is 60-70%, if it is 40% or below then HEART FAILURE

274
Q

these divide into right and left bundles that fire rapidly to allow for simultaneous excitation of the right and left ventricles

A

purkinje fibers (aka subendocardial branches)

275
Q

this travels down the septum between the ventricles and purkinje fibers in the walls of both ventricles
also called atrioventricular bundle

A

bundle of HIS

276
Q

impulse begins here within the right atrium, it is the pacemaker of the heart

A

SA node

277
Q

conduction of heart

A

impulses begin in SA of the right atrium, dottiness down into AV node then down the right and left bundle of HIS to the Purkinje fibers

Patho (4 decks)

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