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Pathophysiology > Final Exam 2 > Flashcards

Final Exam 2 Flashcards

Hemotology, Cardio/Pulm, MSK, Endo/Repro, Digestive

1
Q

<p>total volume of blood ejected by ventricle per minute</p>

A

<p>cardiac output</p>

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2
Q

<p>increased PVR increases what?</p>

A

<p>afterload -> more pressure to push blood out of heart if pressure is higher is system</p>

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3
Q

<p>Increased preload is a result of what?</p>

A

<p>- hypervolemia- renal failure- regurgitation of cardiac valves</p>

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4
Q

<p>Increased afterload is a result of what?</p>

A

<p>- hypertension- vasoconstriction</p>

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5
Q

<p>Explain how increased preload can lead to decreased SV and heart failure</p>

A

<p>- increased preload -> stretching of myocardium -> decreased contractility -> decreased SV + increased ventricular end-diastolic pressure -> pressure backs into pulmonary and venous systems (pulmonary and peripheral edema)</p>

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6
Q

<p>Optimal levels for total cholesterol, LDL, and HDL</p>

A

<p>- total cholesterol: <200 mg/dL- LDL: <100 mg/dL- HDL: >60 mg/dL</p>

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7
Q

<p>Explain the pathophysiology of atherosclerosis</p>

A

<p>- injury to endothelial cells in artery wall -> inflammation- inflammatory process summons macrophages and produces oxygen free radicals- LDL becomes oxidized (causes additional recruitment)- macrophages engulf oxidized LDL -> foam cells- accumulation of foam cells = fatty streak- fatty streak + collagen from injured vessel = fibrous plaque- plaques may occlude blood flow or rupture (rupture initiates clotting and thrombus formation -> ischemia -> infarction)</p>

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8
Q

<p>What usually causes CAD?</p>

A

<p>atherosclerosis (plaque formation)</p>

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9
Q

<p>Explain how coronary occlusion leads to myocardial infarction</p>

A

<p>- myocardial cells become ischemic in 10 seconds of occlusion- cells deprived of glucose needed for aerobic metabolism -> switch to anaerobic (lactic acid accumulation)- heart cells lose ability to contract -> CO decreases</p>

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10
Q

<p>How long can myocardial cells go without O2 before myocardial infarction</p>

A

<p>about 20 minutes</p>

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11
Q

<p>angina caused by gradual luminal narrowing and hardening of arterial walls; consistent type of pain; relieved by rest and nitrates</p>

<p></p>

A

<p>stable angina pectoris</p>

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12
Q

<p>clinical manifestation of stable angina pectoris</p>

A

<p>- transient substernal chest pain (may be mistaken for indigestion)- pallor, diaphoresis, and dyspnea (may all be associated w/ pain)</p>

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13
Q

<p>chest pain attributable to to transient ischemia of myocardium that occurs unpredictably and often at rest; caused by vasospasm of one or more major coronary arteries with or without atherosclerosis</p>

A

<p>prinzmetal angina (varient angina)</p>

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14
Q

<p>2 things linked to silent ischemia</p>

A

<p>DM and chronic stress</p>

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15
Q

<p>angina that is increasing in severity or frequency, new-onset, or at rest; result of reversible myocardial ischemia and is a sign of impending infarction; EKG showsST depression and T wave inversion</p>

A

<p>unstable angina</p>

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16
Q

<p>persistent coronary occlusion leads to infarction of the myocardium closest to the endocardium; EKG showsST depression and T wave inversion without Q waves</p>

A

<p>non-STEMI</p>

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17
Q

<p>continued coronary occlusion that leads to transmural infarction extending from endocardium to pericardium; EKG showsmarked elevations of ST segments</p>

A

<p>STEMI</p>

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18
Q

<p>explain how acute mental stress can lead to MI or sudden cardiac death</p>

A

<p>- stress -> ANS activity -> increased HR, BP and coronary constriction- atherosclerosis or poor LV function -> increased demand and decreased supply- leads to ischemia, plaque rupture, and thrombosis (from platelet activity)- may also cause electrical instability -> VFib/Vtach</p>

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19
Q

<p>classic signs of myocardial infarction</p>

A

<p>- heavy/crushing chest pain- pain may radiate to neck, jaw, back, shoulder, or left arm- N/V- diaphoresis</p>

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20
Q

<p>4 areas of damage caused by HTN</p>

A

<p>- retina- renal disease- CAD/CHF- neurologic disease (stroke, dementia, encephalopathy)</p>

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21
Q

<p>How do the factors leading to HTN cause damage</p>

A

<p>- vasoconstriction -> increased PVR

- renal salt and H2O retention -> increased blood volume
- increased PVR + increased volume -> sustained HTN and vascular remodeling</p>

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22
Q

<p>name 3 acute coronary syndromes (ACS)</p>

A

<p>- unstable angina- non-STEMI- STEMI</p>

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23
Q

<p>ejection fraction <40% and an inability of the heart to generate adequate CO to perfuse tissues</p>

A

<p>heart failure w/ reduced ejection fraction (HFrEF) or systolic HF</p>

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24
Q

<p>Explain how increased PVR can lead to heart failure</p>

A

<p>- increased PVR -> increased afterload (increased resistance to ventricular ejection)- increased workload in LV- increased RAAS and SNS- hypertrophy- increased myocyte demand for O2 (reactive ischemia)- ventricular remodeling- decreased contractility (decreased CO and perfusion of tissues)</p>

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25
Q

<p>symptoms of left heart failure (CHF)</p>

A

<p>- paroxysmal nocturnal dyspnea- cough (w/ frothy/pink-tinged sputum)- orthopnea- exertion dyspnea- fatigue- decreased urine output- edema</p>

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26
Q

<p>Exam findings of left heart failure (CHF)</p>

A

<p>- cyanosis- inspiratory crackles- pleural effusions- HTN or hypotension</p>

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27
Q

<p>pulmonary congestion despite a normal stroke volume and CO; results from increased LVEDP which reflects back into pulmonary and venous system</p>

A

<p>heart failure w/ preserved ejection fraction (HFpEF) or diastolic heart failure</p>

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28
Q

<p>inability of the RV to provide adequate blood flow into pulmonary circulation; usually due to preceding left heart failure</p>

A

<p>right heart failure</p>

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29
Q

<p>clinical manifestations of right heart failure</p>

A

<p>- fatigue- distended jugular veins- ascities- edema- anorexia and GI distress</p>

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30
Q

<p>most common valvular abnormality</p>

A

<p>aortic stenosis</p>

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31
Q

<p>3 causes of aortic stenosis</p>

A

<p>- congenital bicuspid valve degeneration- changes w/ aging- rheumatic heart disease</p>

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32
Q

<p>cardiovascular and pulmonary outcomes of aortic stenosis</p>

A

<p>- LV hypertrophy -> left heart failure- pulmonary edema</p>

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33
Q

<p>most common form of rheumatic heart disease</p>

A

<p>mitral stenosis</p>

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34
Q

<p>valvular abnormalities that cause systolic murmur</p>

A

<p>- aortic stenosis- mitral regurgitation (heard throughout)- tricuspid regurgitation (heard throughout)</p>

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35
Q

<p>valvular abnormalities that cause diastolic murmur</p>

A

<p>- mitral stenosis- aortic regurgitation</p>

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36
Q

<p>painful, red, raised lesions found on the hands and feet. They are associated with a number of conditions, including infective endocarditis, and are caused by immune complex deposition</p>

A

<p>Osler's nodes</p>

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37
Q

<p>non-tender, small erythematous or haemorrhagic macular or nodular lesions on the palms or soles only a few millimeters in diameter that are indicative of infective endocarditis</p>

A

<p>Janeway lesions</p>

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38
Q

<p>systemic, inflammatory disease caused by delayed exaggerated response to infection by group A B-hemolytic streptococcus (pharyngeal infection only)</p>

A

<p>rheumatic fever</p>

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39
Q

<p>antibodies directed against M proteins of streptococci cross-react w/ tissues of heart</p>

A

<p>rheumatic heart disease (RHD)</p>

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40
Q

<p>symptoms of rheumatic fever</p>

A

<p>- fever- lymphadenopathy- N/V and ABD pain- arthralgia - epistaxis- tachycardia</p>

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41
Q

<p>Risk factors for introduction of bacteria into endocardium</p>

A

<p>- dental, GU, or cardiac procedures- skin, wound, lung, or GU infections- indwelling catheters- injection drug use</p>

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42
Q

<p>signs and symptoms of infective endocarditis once vegetation forms</p>

A

<p>- fever, night sweats, malaise, weight loss- heart murmurs and failure- embolization of vegetation -> abscesses, petechiae, splinter hemorrhages, Osler nodules, and Janeway lesions, right-side emboli = PE; left-side emboli = stroke</p>

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43
Q

<p>What is missing from cells in all types of shock? What is a common finding in all types of shock?</p>

A

<p>- oxygen (either not receiving or not able to use it)- decreased CO</p>

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44
Q

<p>Describe the effects of impaired O2 delivery and use in shock</p>

A

<p>- no O2 -> anaerobic metabolism -> decrease ATP and increase lactic acid- increased lactic acid -> metabolic acidosis- decrease ATP -> decrease Na/K pump -> increased intracellular volume (cellular edema) -> decreased circulatory volume- cellular edema -> lysosomal enzymes -> inflammation and activation of clotting cascade</p>

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45
Q

<p>Describe the effects of impaired glucose delivery and use in shock</p>

A

<p>- increased serum cortisol, thyroid hormone, and catecholamines -> increased lipolysis, gluconeogenesis, and glycogenolysis- lypolysis = increased serum triglycerides- glycogenolysis = decreased energy stores- gluconeogenesis = proteins used for fuel, decrease albumin and increased urea and ammonia formation- muscle wasting and build up of metabolic products</p>

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46
Q

<p>How does the body compensate for shock</p>

A

<p>- decrease CO and tissue perfusion -> SNS activation- increased BP, HR, and contractility - RAAS activation (retain Na and H2O to increase preload)- vasoconstriction and activation of ADH -> increase preload- increased volume and CO -> restoration of perfusion</p>

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47
Q

<p>4 types of shock</p>

A

<p>- hypovolemic- cardiogenic- distributive- obstructive</p>

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48
Q

<p>decreased CO and evidence tissue hypoxia in the presence of adequate intravascular volume (heart cannot contract effectively; fluid volume not affected)</p>

A

<p>cardiogenic shock</p>

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49
Q

<p>causes of cariogenic shock</p>

A

<p>direct pump failure- MI, cardiac arrest- ventricular dysrhythmia</p>

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50
Q

<p>signs and symptoms of cardiogenic shock</p>

A

<p>- confusion- tachycardia- hypotension- tachypnea- venous and pulmonary edema- oliguria (urine output < 30mL/hour)- dusky skin color; skin cold and clammy</p>

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51
Q

<p>caused by loss of whole blood (hemorrhage), plasma (burns), or interstitial fluid (diaphoresis, DM, DI, emesis, diarrhea, or diuresis) in large amounts</p>

A

<p>hypovolemic shock</p>

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52
Q

<p>signs and symptoms of hypovolemic shock</p>

A

<p>- hypotension- tachypnea- tachycardia (weak pulse)- hypoxia- decreased/absent urine- thirst, agitation, anxiety, confusion- skeletal muscle weakness- cold, clammy, cyanotic skin</p>

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53
Q

<p>shock due to decreased vascular volume or tone -> vasodilation w/ pooling causes decrease preload, SV, and CO</p>

A

<p>distributive shock</p>

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54
Q

<p>3 types of distributive shock</p>

A

<p>- neurogenic shock- anaphylactic shock- septic shock</p>

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55
Q

<p>result of widespread and massive vasodilation due to parasympathetic overstimulation and sympathetic understimulation</p>

A

<p>neurogenic/vasogenic shock</p>

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56
Q

<p>results from widespread hypersensitivity reaction known as anaphylaxis</p>

A

<p>anaphylactic shock</p>

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57
Q

<p>signs and symptoms of anaphylactic shock</p>

A

<p>- vasodilation and increase capillary permeability (due to histamine) -> hypovolemia- decreased contractility and dysrhythmia- bronchial edema and pulmonary obstruction- widespread hypoxia</p>

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58
Q

<p>toxins and endotoxins related into blood cause systemic inflammatory response syndrome (SIRS); metabolism becomes anaerobic due to decreased MAP, clot formation in capillaries, and poor cellular uptake of O2</p>

A

<p>septic shock</p>

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59
Q

<p>signs of sepsis</p>

A

<p>- bacteremia + SIRS- SIRS: fever, tachycardia, tachypnea, leukocytosis</p>

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60
Q

<p>septic shock is related to what clotting abnormality</p>

A

<p>DIC</p>

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61
Q

<p>shock due to indirect pump failure (cardiac tamponade, or PE); cardiac function decreases by non-cardiac factors (total body fluid not affected)</p>

A

<p>obstructive shock</p>

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62
Q

<p>signs of cardiac tamponade</p>

A

<p>- JVD- paradoxical pulse- decrease CO- muffled heart sounds</p>

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63
Q

<p>progressive dysfunction of 2 or more organ systems resulting from an uncontrolled inflammatory response to severe illness or injury; most commonly caused by septic shock</p>

A

<p>multiple organ dysfunction syndrome (MODS)</p>

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64
Q

<p>Explain pathogenesis of MODS</p>

A

<p>- injury/sepsis/trauma -> neuroendocrine response and release of inflammatory mediators- activation of complement, coagulation, and kinin systems (massive systemic inflammatory response)- hypermetabolism- vasodilation and selective vasoconstriction -> maldistribution of blood flow -> hypoperfusion and decreased CO- hypermetabolism and hypo perfusion -> increased O2 demand -> tissue hypoxia/metabolic failure -> acidosis- organ dysfunction</p>

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65
Q

<p>autoimmune condition characterized by formation of thrombi filled w/ inflammatory and immune cells; strongly associated w/ smoking</p>

A

<p>Buergers disease</p>

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66
Q

<p>pain w/ ambulation due to gradually increasing obstruction of arterial blood flow to the legs by atherosclerosis in the iliofemoral vessels; seen in arterial PVD</p>

A

<p>intermittent claudication</p>

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67
Q

<p>3 factors that promote venous thrombosis (triad of Virchow)</p>

A

<p>- venous stasis (immobility, age, CHF)- venous endothelial damage (trauma, IV meds)- hypercoagulable states (inherited disorders, pregnancy, malignancy, OCP, or HRT)</p>

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68
Q

<p>6 Ps of acute arterial occlusion</p>

A

<p>- Pain- Paresthesias- Paralysis- Pallor- Pulselessness- Perishingly cold/Poikilothermia</p>

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69
Q

<p>Explain the rhythm of Cheyne-Stokes respirations</p>

A

<p>- increased levels of CO2 -> tachypnea- CO2 levels decrease -> leads to apnea until CO2 accumulates again</p>

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70
Q

<p>PaCO2 is greater than 44 mmHg</p>

A

<p>hypercapnia (increased CO2 levels) -> leads to respiratory acidosis</p>

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71
Q

<p>PaCO2 less than 36 mmHg</p>

A

<p>hypocapnia (decreased CO2 levels) -> leads to respiratory alkalosis</p>

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72
Q

<p>7 causes of hypercapnia</p>

A

<p>- depression of respiratory center by drugs- diseases of the medulla- abnormalities of spinal conducting pathways (spinal cord disruption)- diseases of NMJ or respiratory muscles (MG or MD)- thoracic cage abnormalities- large airway obstruction (tumors/sleep apnea)- increased work of breathing or physiologic dead space</p>

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73
Q

<p>pathological condition which results when the alveoli of the lungs are perfused (Q) with blood as normal, but ventilation (the supply of air or V) fails to supply the perfused region -> low V/Q</p>

A

<p>pulmonary shunt</p>

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74
Q

<p>V/Q mismatching results in what?</p>

A

<p>hypoxemia</p>

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75
Q

<p>air pressure in the pleural space = barometric pressure; air drawn into pleural space on inspiration is forced out on expiration</p>

A

<p>open (communicating) pneumothorax</p>

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76
Q

<p>one-way valve that permits air to enter on inspiration but prevents escape during expiration (causes mediastinal shift) -> life threatening</p>

A

<p>tension pneumothorax</p>

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77
Q

<p>Name 5 types of pleural effusion drainage</p>

A

<p>- transudative (hydrothorax): watery drainage from intact capillaries- exudative: WBC and protein- empyema: pus-like drainage- hemothorax: bloody drainage- chylothorax: milky lymphatic drainage and fat droplets</p>

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78
Q

<p>diseases characterized by airway obstruction that is worse w/ expiration (more force is required to expire a given volume of air and emptying of the lungs is slowed)</p>

A

<p>obstructive lung diseases</p>

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79
Q

<p>3 most common obstructive lung diseases</p>

A

<p>- asthma- emphysema- chronic bronchitis</p>

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80
Q

<p>Describe an acute asthmatic response</p>

A

<p>- inhaled Ag binds to mast cells covered w/ preformed IgE- mast cells release mediators- mediators induce bronchospasm, edema from increased capillary permeability, and mucous secretion (goblet cells)- dendritic cells process and present Ag to Th2 -> produce ILs- eosinophils activated -> damage respiratory epithelium - neutrophils add to inflammation and airway obstruction</p>

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81
Q

<p>clinical manifestations of asthma attack</p>

A

<p>- chest constriction- expiratory wheezing- dyspnea- nonproductive cough- prolonged expiration- tachycardia- tachypnea</p>

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82
Q

<p>decrease in systolic BP during inspiration of more than 10 mmHg; may be seen during asthma attack</p>

A

<p>pulses paradoxus</p>

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83
Q

<p>COPD includes what 2 disorders</p>

A

<p>chronic bronchitis and emphysema</p>

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84
Q

<p>hyper-secretion of mucus and chronic productive cough for at least 3 months of the year for at least 2 consecutive years</p>

A

<p>chronic bronchitis</p>

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85
Q

<p>pathogenesis of chronic bronchitis</p>

A

<p>- chronic irritation from inhaled substances/irritants such as tobacco smoke- inflammation causes bronchial edema, hyper-secretion of mucus (goblet cells), and smooth muscle hypertrophy w/ fibrosis, and bacterial colonization of airways</p>

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86
Q

<p>clinical manifestation of chronic bronchitis</p>

A

<p>- productive cough (classic)- prolonged expiration- cyanosis- chronic hypoventilation- polycythemia- cor pulmonale</p>

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87
Q

<p>abnormal permanent enlargement of gas-exchange airways accompanied by destruction of alveolar walls without obvious fibrosis</p>

A

<p>emphysema</p>

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88
Q

<p>primary emphysema is inherited and linked to what deficiency</p>

A

<p>a1-antitrypsin deficiency</p>

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89
Q

<p>pathogenesis of emphysema</p>

A

<p>- destruction of alveoli through breakdown of elastin within the septa (increased protease activity)- loss of elastin = loss of recoil of bronchial walls- produces large air spaces within lung parenchyma (bullae)</p>

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90
Q

<p>mucous plugs and narrowed airways cause \_\_\_\_; leads to hyperinflation of alveoli and hyper-expansion of chest</p>

A

<p>air trapping</p>

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91
Q

<p>clinical manifestations of emphysema</p>

A

<p>- dyspnea- wheezing- barrel chest (classic)- prolonged expiration</p>

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92
Q

<p>diseases characterized by decreased compliance of lung tissue (takes more effort to expand lungs during inspiration)</p>

A

<p>restrictive lung disease</p>

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93
Q

<p>autosomal recessive defect on chromosome 7 that causes defective epithelial chloride ion transport and deficient Na in airways, bile ducts, pancreas, and sweat ducts</p>

A

<p>cystic fibrosis</p>

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94
Q

<p>3 causes of pulmonary edmea</p>

A

<p>- left heart failure: causes increased pulmonary capillary hydrostatic pressure- injury to capillary endothelium: movement of fluid and protein from capillary to alveoli- blockage of lymphatics: inability to remove excess fluid from interstitial space</p>

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95
Q

<p>Pathogenesis of ARDS</p>

A

<p>- acute lung injury -> inflammation and neutrophil aggregation w/ release of mediators and complement- platelet activation -> micro thrombi in pulmonary circulation -> decreased flow to lungs -> pulmonary HTN and V/Q mismatch- damage to alveolar and endothelial cells -> disrupts alveolocapillary membrane -> fluid enters interstitial space -> impaired surfactant production and atelectasis</p>

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96
Q

<p>3 phases of ARDS</p>

A

<p>- exudative phase: pulmonary edema and hemorrhage w/ severe impairment of ventilation- proliferative phase: proliferation of type II pneumocytes; formation of hyaline membrane- fibrotic phase: tissue remodeling (destruction of alveoli and bronchioles)</p>

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97
Q

<p>Final result of ARDS</p>

A

<p>acute respiratory failure- hypoxemia- hypercapnia- acidosis</p>

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98
Q

<p>pathologic course of pneumonia</p>

A

<p>- aspiration of bacteria -> adherence to alveolar macrophages- inflammatory response - consolidation of lung parenchyma- leukocyte infiltration (neutrophils and macrophages)- phagocytosis in alveoli- resolution of infection</p>

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99
Q

<p>clinical manifestation of PE</p>

A

<p>sudden onset of symptoms - pleuritic chest pain - dyspnea - tachypnea - tachycardia - cough/hemoptysis- unexplained anxiety/sense of doom - massive occlusion = pulmonary HTN and shock</p>

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100
Q

<p>mean pulmonary A. pressure greater than 25 mmHg at rest</p>

A

<p>pulmonary artery HTN (PAH)</p>

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101
Q

<p>PAH is associated w/ what conditions</p>

A

<p>- COPD- interstitial fibrosis- obesity-hypoventilation syndrome</p>

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102
Q

<p>pathogenesis of PAH</p>

A

<p>- conditions cause chronic hypoxemia and chronic acidosis - Pulmonary A. vasoconstriction - increased pulmonary A. pressure - intimal fibrosis and hypertrophy of medial smooth muscle layer of pulmonary As.</p>

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103
Q

<p>right ventricular enlargement caused by PAH</p>

A

<p>cor pulmonale</p>

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104
Q

<p>Explain how PAH causes cor pulmonale</p>

A

<p>- resistance and pressure in pulmonary A. increases- workload of RV increases- leads to hypertrophy of RV and right heart failure</p>

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105
Q

<p>non-small cell lung cancer that usually originates in the peripheral regions of pulmonary parenchyma; moderate growth rate</p>

A

<p>adenocarcinoma</p>

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106
Q

<p>neuroendocrine lung cancer that has the highest correlation w/ smoking and arise centrally (hilar/mediastinal); very rapid growing and poor prognosis</p>

A

<p>small cell carcinoma</p>

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107
Q

<p>3 conditions associated w/ pulmonary shunting/low V/Q</p>

A

<p>low ventilation of perfused areas- atelectasis- asthma- pulmonary edema</p>

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108
Q

<p>1 condition associated w/ alveolar dead space/high V/Q</p>

A

<p>pulmonary emboli</p>

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109
Q

<p>2 conditions associated w/ alveolar capillary membrane barrier slowing diffusion of O2</p>

A

<p>- emphysema: decrease surface area- chronic bronchitis: thickened alveolar capillary membrane w/ edema and fibrosis</p>

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110
Q

<p>Formation of fibrous tissue or nodules in the lungs due to chronic environmental exposure</p>

A

<p>pneumoconiosis</p>

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111
Q

<p>Types of people at high risk for pneumonia and TB</p>

A

<p>- nursing home pts- prisoners- COPD- TB = pneumonia + pts w/ HIV</p>

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112
Q

<p>5 types of incomplete fractures</p>

A

<p>- greenstick- torus- bowing- stress- transchondral</p>

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113
Q

<p>break in one cortex of bone with splintering of inner bone surface; commonly occurs in children and elderly</p>

A

<p>greenstick fracture</p>

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114
Q

<p>buckling of cortex of a bone</p>

A

<p>torus fracture</p>

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115
Q

<p>bending of a bone</p>

A

<p>bowing fracture</p>

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116
Q

<p>diseases that cause pathologic fractures</p>

A

<p>- osteoporosis- RA- Paget disease- osteomalacia- rickets- hyperparathyroidism- radiation therapy- cancer- infection</p>

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117
Q

<p>healing that occurs when adjacent bone cortices are in contact with one another; usually due to surgical fixation and restriction of movement between fragments</p>

A

<p>direct/primary healing</p>

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118
Q

<p>healing that involves both intramembranous and endochondral bone formation, development of callus, and bone remodeling; occurs in fractures that are treated with non-rigid or semi-rigid bone fixation (casts, braces, etc.)</p>

A

<p>indirect/secondary healing</p>

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119
Q

<p>List the 5 steps of callus formation</p>

A

<p>- hematoma formation- organization of hematoma into fibrous network- invasion of osteoblasts; lengthening of collagen strands and deposition of calcium -callus formation -remodeling: excess callus is reabsorbed and trabecular bone is deposited</p>

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120
Q

<p>lateral epicondylitis</p>

A

<p>tennis elbow</p>

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121
Q

<p>medial epicondylitis</p>

A

<p>golfer's elbow</p>

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122
Q

<p>rapid breakdown of muscle that causes release of intracellular contents, including protein pigment myoglobin, into the extracellular space and bloodstream</p>

A

<p>rhabdomyolysis (myoglobinuria)</p>

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123
Q

<p>Classic triad of rhabdomyolysis</p>

A

<p>- muscle pain- weakness- dark urine (sometimes only thing present)</p>

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124
Q

<p>Most important lab value for rhabdomyolysis</p>

A

<p>serum creatinine kinase (CK) level</p>

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125
Q

<p>Normal CK level</p>

A

<p>- men: 5-25- women: 5-35</p>

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126
Q

<p>causes of rhabdomyolysis</p>

A

<p>- electrical injury/burns- blunt trauma- drugs (EtOH, PCP, amphetamines, heroin, cocaine)- DKA- heat stroke- status epilepticus - tetanus- strenuous exercise</p>

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127
Q

<p>Goals of treatment for rhabdomyolysis</p>

A

<p>maintaining adequate urinary flow (IV hydration) and prevention of kidney failure</p>

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128
Q

<p>causes of compartment syndrome</p>

A

<p>- bleeding after fracture (increases pressure)- decrease compartment volume (tight bandage or cast)- combination both conditions</p>

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129
Q

<p>Explain the pathophysiology of compartment syndrome</p>

A

<p>- limb compression -> local pressure -> tamponade- muscle/capillary necrosis- edema -> rising compartment pressure -> compartment tamponade- muscle ischemia/infarction- neural injury -> Volkmann ischemic contracture</p>

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130
Q

<p>explain pathophysiology of crush syndrome</p>

A

<p>- muscle infarction due to compartment syndrome- myoglobinemia -> renal failure- ECF shift -> shock - acidosis/hyperkalemia -> cardiac dysrhythmia</p>

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131
Q

<p>causes of osteoporosis</p>

A

<p>- decreased levels of estrogen (main hormone) and testosterone - decreased activity level- inadequate levels of vitamin D, C, and Mg</p>

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132
Q

<p>causes of osteomalacia</p>

A

<p>- deficiency of vitamin D -> lowers absorption of calcium from intestines</p>

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133
Q

<p>clinical manifestations of osteomalacia</p>

A

<p>- pain- bone fractures- vertebral collapse- bone malformations (bowed legs or "knock-knees")- muscular weakness -> waddling gait</p>

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134
Q

<p>state of increased metabolic activity in bone characterized excessive resorption of spongy bone and accelerated formation of softened bone; usually affects the axial skeleton</p>

A

<p>Paget disease</p>

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135
Q

<p>bone infection most often caused by staphylococcal infection</p>

A

<p>osteomyelitis</p>

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136
Q

<p>clinical manifestations of osteomyelitis</p>

A

<p>- acute/chronic inflammation- fever- pain- necrotic bone</p>

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137
Q

<p>Treatment for osteomyelitis</p>

A

<p>- antibiotics- debridement- surgery- hyperbaric O2 therapy</p>

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138
Q

<p>manifestation of OA</p>

A

<p>- pain- stiffness- enlargement of joint- tenderness- limited ROM- deformity</p>

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139
Q

<p>What is activated in RA that develop an exaggerated immune response?</p>

A

<p>synovial fibroblasts (SFs)</p>

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140
Q

<p>main 2 classes of immunoglobulins that are part of rheumatoid factors (RF)</p>

A

<p>- IgM and IgG- occasionally IgA</p>

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141
Q

<p>What will be present in joint fluid with RA?</p>

A

<p>inflammatory exudate</p>

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142
Q

<p>Explain the pathogenesis of RA</p>

A

<p>- CD4 T helper cells and others in synovial fluid activated -> release cytokines- activation of B lymphocytes -> formation of RF -> formation of autoimmune complexes and probable deposition in joint tissue- inflammatory cytokine release- RANKL release and osteoclast activation- angiogenesis in the synovium</p>

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143
Q

<p>Pt is said to have RA if the have 4 or more of the following:</p>

A

<p>- morning joint stiffness- arthritis in 3 or more joints- arthritis in hand joints- symmetric arthritis- rheumatoid nodules- abnormal amounts of serum RF- radiographic changes</p>

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144
Q

<p>explain the pathophysiology of ankylosing spondylitis</p>

A

<p>- inflammation of fibrocartilage (mainly in vertebrae and sacroiliac joint)- inflammatory cells infiltrate and erode fibrocartilage - repair begins -> scar tissue ossifies and calcifies - joint eventually fuses</p>

145
Q

<p>when uric acid crystals occur in synovial fluid</p>

A

<p>gouty arthritis</p>

146
Q

<p>type of metabolism gout is related to</p>

A

<p>purine (adenine and guanine) metabolism -> uric acid is end product</p>

147
Q

<p>3 stages of gout</p>

A

<p>- asymptomatic hyperuricemia- acute gouty arthritis- tophaceous gout</p>

148
Q

<p>stage of gout; serum urate level is elevated but arthritic symptoms, tophi, and renal stones not present</p>

A

<p>asymptomatic hyperuricemia</p>

149
Q

<p>stage of gout; attacks develop w/ increased serum urate concentrations; tends to occur w/ sudden/sustained increases in hyperuricemia but can be triggered by trauma, drugs, and alcohol</p>

A

<p>acute gouty arthritis</p>

150
Q

<p>stage of gout; progressive inability to excrete uric acid expands to curate pool until monosodium rate crystal deposits (tophi) appear in cartilage, synovial membrane, tendons, and soft tissue</p>

A

<p>tophaceous gout</p>

151
Q

<p>associated w/ chronic anxiety</p>

A

<p>stress induced muscle tension</p>

152
Q

<p>chronic widespread joint and muscle pain with associated increased sensitivity to touch, absence of inflammation, fatigue, and sleep disturbances</p>

A

<p>fibromyalgia (FM)</p>

153
Q

<p>Where are majority of osteosarcomas found?</p>

A

<p>located in the metaphyses of long bones; about half occur around the knees</p>

154
Q

<p>malignant tumor of striated muscle; highly malignant w/ rapid metastasis</p>

A

<p>rhabdomyosarcoma</p>

155
Q

<p>What muscles most commonly develop rhabdomyosarcoma?</p>

A

<p>- tongue, neck, larynx, nasal cavity, axilla, vulva, and heart</p>

156
Q

<p>List the 7 hormones released from the anterior pituitary and their target tissues</p>

A

<p>- Prolactin (mammary gland)- ACTH (adrenal cortex)- GH (bone/muscle/tissues)- TSH (thyroid gland)- LH + FSH (ovaries and testes)- MSH (melanin in skin)</p>

157
Q

<p>Acromegaly vs gigantism</p>

A

<p>- acromegaly: occurs in adults (after growth plates have close)- gigantism: occurs in childhood (before growth plates close)</p>

158
Q

<p>form of thyrotoxicosis in which excess amounts of TH are secreted from the thyroid gland</p>

A

<p>hyperthyroidism</p>

159
Q

<p>clinical manifestations of hyperthyroidism</p>

A

<p>- thin hair- tachycardia- weight loss (elevated metabolism)- exophthalmos (protruding eyes)- hyperreflexia - enlarged thyroid</p>

160
Q

<p>over secretion of T3/T4 due to abnormal antibodies (TSIs) that stimulate TSH receptors (type II hypersensitivity)</p>

A

<p>Grave's disease</p>

161
Q

<p>What causes goiters?</p>

A

<p>thyroid enlargement due to iodine deficiency - follicles make thyroglobulin but cannot make TH</p>

162
Q

<p>dangerous worsening of thyrotoxic state in which death can occur within 48 hours without treatment; sxs caused by increased action of T4 and T3 exceeding metabolic demands</p>

A

<p>thyrotoxic crisis (thyroid storm)</p>

163
Q

<p>Sxs of thyrotoxic crisis</p>

A

<p>- hyperthermia- tachycardia- high output heart failure- agitation/delirium- N/V/D</p>

164
Q

<p>clinical manifestation of cretinism</p>

A

<p>- difficulty eating- protruding tongue- hypotonia- lethargy- bradycardia- cognitive disability varies</p>

165
Q

<p>most common form of primary hypothyroidism; gradual inflammatory destruction of thyroid tissue by infiltration of auto reactive T lymphocytes and circulating thyroid antibodies</p>

A

<p>autoimmune thyroiditis (Hashimoto's thyroiditis)</p>

166
Q

<p>clinical manifestations of hypothyroidism</p>

A

<p>- loss of hair- bradycardia- decreased metabolism- lethargy- cold intolerance- muscle weakness- LE edema</p>

167
Q

<p>characteristic sign of severe or long-standing hypothyroidism; will see non pitting, boggy edema (around eyes, hands, feet, and supraclavicular fossa), slurred speech, and hoarseness</p>

A

<p>myxedema</p>

168
Q

<p>clinical manifestation of myxedema coma (medical emergency)</p>

A

<p>- hypothermia w/o shivering- hypoventilation- hypotension- hypoglycemia - lactic acidosis</p>

169
Q

<p>high levels of ADH in the absence of normal physiologic stimuli for release</p>

A

<p>syndrome of inappropriate ADH secretion (SIADH)</p>

170
Q

<p>How does SIADH affect the following:- urine output- urine osmolality- serum Na- serum osmolality</p>

A

<p>- urine output: low- urine osmolality: high- serum Na: low (hyponatremia)- serum osmolality: low (hypoosmolar)</p>

171
Q

<p>symptoms of SIADH</p>

A

<p>- water retention - low urine output- N/V- mental changes</p>

172
Q

<p>failure of hypothalamus to produce ADH or release it from posterior pituitary; decrease in ADH plasma levels</p>

A

<p>neurogenic/central diabetes insipidus (DI)</p>

173
Q

<p>kidneys unable to respond to ADH; increase plasma ADH</p>

A

<p>nephrogenic diabetes insipidus (DI)</p>

174
Q

<p>How does DI affect the following:- urine output- urine osmolality- serum Na- serum osmolality</p>

A

<p>- urine output: high- urine osmolality: low- serum Na: high (hypernatremia)- serum osmolality: high (hyperosmolar)</p>

175
Q

<p>symptoms of DI</p>

A

<p>- polyuria- thirst- high urine output- signs of dehydration</p>

176
Q

<p>treatment of SIADH</p>

A

<p>- fluid restriction- treat the cause</p>

177
Q

<p>characterized by greater than normal secretion of PTH and hypercalcemia</p>

A

<p>hyperparathyroidism</p>

178
Q

<p>How does hyperparathyroidism affect Ca and Pi</p>

A

<p>- increased Ca levels (hypercalcemia) -> increases bone resorption to release Ca and GI reabsorption- decreased Pi levels (hypophosphatemia) -> PTH causes Pi to be excreted in urine</p>

179
Q

<p>clinical manifestations of primary hyperparathyroidism</p>

A

<p>- fatigue- headache- depression- anorexia- N/V- pathologic fractures</p>

180
Q

<p>How does hypoparathyroidism affect Ca and Pi</p>

A

<p>- decreased Ca levels (hypocalcemia)- increased Pi levels (hyperphosphatemia)</p>

181
Q

<p>clinical manifestations of hypoparathyroidism</p>

A

<p>- symptoms of hypocalcemia (ex. tetany and muscle spasms)- dry skin- loss of body and scalp hair- hypoplasia of developing teeth- bone deformities</p>

182
Q

<p>refers to clinical manifestations resulting from chronic exposure to excess cortisol regardless of cause</p>

A

<p>Cushing syndrome</p>

183
Q

<p>clinical manifestations of Cushing's syndrome</p>

A

<p>- fat deposition on neck/back (buffalo hump)- fat deposition on the face (moon face)- ABD fat deposition- bruising (breakdown of collagen)- stretch marks- muscle weakness/wasting- osteoporosis- adrenal hyperplasia</p>

184
Q

<p>How would Cushing disease affect the following values:- K- Na- glucose</p>

A

<p>- K: hypokalemia (aldosterone -> K excretion)- Na: hypernatremia (aldosterone -> Na reabsorption)- glucose: hyperglycemia (high cortisol)</p>

185
Q

<p>primary adrenal insufficiency (hyposecretion of all adrenal steroids) usually due to autoimmune restriction of adrenal gland</p>

A

<p>Addison's disease</p>

186
Q

<p>How would Addison's disease affect the following values:- K- Na- glucose</p>

A

<p>- K: hyperkalemia (no aldosterone for K excretion)- Na: hyponatremia (no aldosterone for Na reabsorption)- glucose: hypoglycemia (low cortisol)</p>

187
Q

<p>clinical manifestations of Addison's diseases</p>

A

<p>- weakness/fatigue- skin hyperpigmentation (due to high MSH associated w/ high ACTH)- hypotension - tachycardia- N/V/D- adrenal atrophy</p>

188
Q

<p>hyper-secretion of aldosterone due to adrenal neoplasm</p>

A

<p>primary hyperaldosteronism (Conn syndrome)</p>

189
Q

<p>Symptoms of pheochromocytoma</p>

A

<p>- persistant HTN- headache- pallor- diaphoresis- tachycardia/palpitations- anxiety</p>

190
Q

<p>lab value diagnosis criteria for DM</p>

A

<p>- HbA1c > 6.5%- fasting plasma glucose (FPG) > 126 mg/dl (fasting = at least 8 hours)- 2 hour plasma glucose > 200 mg/dl during oral glucose tolerance test (OGTT)- symptoms of hyperglycemia w/ random plasma glucose > 200 mg/dl</p>

191
Q

<p>Describe pathophysiology of IDDM</p>

A

<p>- autoantigens form on B-cells and circulate in bloodstream/lymphatics- activation of cellular immunity (T cells) and humoral immunity (autoantibodies) towards B-cells- destruction of B-cells with decreased insulin secretion</p>

192
Q

<p>clinical manifestations of IDDM</p>

A

<p>- polydipsia (water attracted to glucose -> intracellular dehydration)- polyuria (hyperglycemia = osmotic diuretic)- polyphagia (depletion of cellular stores due to lack of glucose -> starvation)- weight loss- fatigue- visual changes- paresthesias</p>

193
Q

<p>What is one of the most important contributors to insulin resistance and NIDDM</p>

A

<p>obesity</p>

194
Q

<p>clinical manifestations of NIDDM</p>

A

<p>- some classic sxs (polyuria/polydipsia)- fatigue- pruritus- recurrent infections- visual changes- neuropathy- individual is usually overweight w/ dyslipidemia and HTN</p>

195
Q

<p>low blood glucose during the night that may lead to rise in morning blood glucose; tx is a nighttime snack to prevent hypoglycemia</p>

A

<p>Somogyi effect</p>

196
Q

<p>early morning rise in blood glucose level related to release of GH, cortisol, and catecholamines w/o preceding hypoglycemia; tx is insulin to counter hyperglycemia</p>

A

<p>dawn phenomenon</p>

197
Q

<p>symptoms of hypoglycemia</p>

A

<p>- pallor- tremor- tachycardia/palpitations- diaphoresis - headache- irritability/anxiety- confusion- seizures- coma</p>

198
Q

<p>serious complication related to deficiency of insulin and increase in levels of insulin couter-regulatory hormones (catecholamines, GH, cortisol, and glucagon)</p>

A

<p>diabetic ketoacidosis (DKA)</p>

199
Q

<p>3 main characteristics of DKA</p>

A

<p>- hyperglycemia- acidosis- ketonuria</p>

200
Q

<p>Why is DKA more common in IDDM?</p>

A

<p>insulin is more deficient</p>

201
Q

<p>Pathophysiology of DKA</p>

A

<p>- w/ insulin deficiency -> lipolysis is enhanced (increased fatty acid delivery to liver)- increased glyconeogenesis (contribute to hyperglycemia and production of ketone bodies)- increased ketones -> decreased pH -> metabolic acidosis</p>

202
Q

<p>clinical manifestations of DKA</p>

A

<p>- Kussmaul respirations- fruity/acetone odor in breath- CNS depression- ketonuria- anorexia- N/V and ABD pain- postural dizziness</p>

203
Q

<p>more common complication of NIDDM that differs from DKA w/ higher degree of fluid deficiency rather than insulin deficiency</p>

A

<p>hyperosmolar hyperglycemic nonketoic syndrome (HHNKS)</p>

204
Q

<p>In which disease are glucose levels higher: DKA or HHNKS?</p>

A

<p>HHNKS -> due to volume depletion</p>

205
Q

<p>clinical manifestations of HHNKS</p>

A

<p>- severe dehydration (from polyuria)- loss of electrolytes (ex. potassium)- neurologic changes (stupor, coma, seizures)- hypotension/hypoperfusion/tachycardia- N/V and ABD pain</p>

206
Q

<p>clinical manifestation of diabetic neuropathy</p>

A

<p>- glove and stocking loss of sensation- loss of motor nerve function w/ clawed toes and small muscle wasting in hands- Charcot joints (joint and ligament degeneration; mainly in feet)</p>

207
Q

<p>How does diabetic neuropathy lead to amputation?</p>

A

<p>- decrease in sensation -> painless trauma -> ulceration -> infection- muscle atrophy -> changes in gait -> new pressure points -> ulceration -> infection- autonomic neuropathy -> decreased perspiration -> dry skin/cracks/fissures -> infection- All lead to soft tissue infection and osteomyelitis</p>

208
Q

<p>5 main reasons diabetics have increased risk for infection throughout the body</p>

A

<p>- impaired senses (neuropathy and retinopathy)- hypoxia (glycosylated Hgb impaired O2 delivery to tissues)- pathogens (some proliferate rapidly due to high glucose levels)- blood supply (vascular changes and reduced supply of WBCs)- suppressed immune response (impaired innate and adaptive immune system)</p>

209
Q

<p>rare form of dysphagia related to loss of inhibitory neurons in the myenteric plexus w/ smooth muscle atrophy in the middle/lower parts of esophagus</p>

A

<p>achalasia</p>

210
Q

<p>What does achalasia lead to?</p>

A

<p>altered esophageal peristalsis and failure of lower esophageal sphincter (LES) to relax -> can cause distention/obstruction in esophagus</p>

211
Q

<p>type of diaphragmatic hernia w/ protrusion of the upper part of the stomach through the diaphragm into the thorax</p>

A

<p>hiatal hernia</p>

212
Q

<p>proximal portion of stomach moves into the thoracic cavity through the esophageal hiatus</p>

A

<p>sliding hiatal hernia (type 1; most common)</p>

213
Q

<p>herniation of the greater curvature of the stomach through a secondary opening in the diaphragm alongside the esophagus</p>

A

<p>paraesophageal hiatal hernia (type 2)</p>

214
Q

<p>narrowing or blocking of the opening between the stomach and the duodenum (can be congenital or acquired)</p>

A

<p>pyloric obstruction (gastric outlet obstruction)</p>

215
Q

<p>most common acquired cause of pyloric obstruction</p>

A

<p>- peptic ulcer disease or carcinoma near pylorus- duodenal ulcers more likely to cause obstruction</p>

216
Q

<p>7 common causes of intestinal obstruction</p>

A

<p>- hernia- intussusception - torsion (volvulus)- diverticulosis- tumors- paralytic ileus- fibrous adhesions (post-op; Crohn's)</p>

217
Q

<p>most common type of bowel obstruction</p>

A

<p>small bowel obstruction (SBO)</p>

218
Q

<p>How would a bowel obstruction lead to pneumonia?</p>

A

<p>- distention -> pressure on diaphragm -> decreased respiratory volume -> atelectasis -> pneumonia</p>

219
Q

<p>How would a bowel obstruction lead to peritonitis?</p>

A

<p>- distention and prolonged increased of wall tension -> decreased venous return -> bowel edema -> increased capillary permeability (fluid loss into peritoneum) -> bacterial translocation to peritoneum</p>

220
Q

<p>How would a bowel obstruction lead to loss of water/electrolytes and dehydration?</p>

A

<p>- ABD pain leads to N/V, decreased intake, decreased nutrient absorption, and decreased carb reserves (ketosis)</p>

221
Q

<p>What 2 electrolytes are affected most by a bowel obstruction?</p>

A

<p>- K (hypokalemia)- Cl (hypochloremia)</p>

222
Q

<p>How would a bowel obstruction lead to shock?</p>

A

<p>- distention -> increased capillary permeability - dehydration from loss of water/electrolytes- both lead to hypovolemia -> shock</p>

223
Q

<p>2 most common causes of ulcers</p>

A

<p>NSAIDs and H. Pylori infection (both are erosive factors)</p>

224
Q

<p>most common type of peptic ulcer</p>

A

<p>duodenal ulcer (also caused by NSAIDs and H. Pylori)</p>

225
Q

<p>How do gastric ulcers form?</p>

A

<p>- caused H. Pylori, NSAIDS, bile salts, alcohol, or ischemia- damage to mucosal barrier -> decreased function of mucosal cells -> diffusion of acid into gastric mucosa- formation of histamine -> increased acid production, increased capillary permeability and mucosal edema- conversion of pepsinogen to pepsin causes further erosion and bleeding -> ulcer</p>

226
Q

<p>Consequences of upper and lower GI bleeding</p>

A

<p>- blood volume depletion -> decreased CO -> compensatory constriction of peripheral arteries- decreased blood flow to kidneys (renal failure)- decreased blood flow to GI structures -> bowel/liver infarction/necrosis- decreased blood flow to brain and heart- metabolic acidosis -> lactic acidosis -> death</p>

227
Q

<p>Chief problem of pancreatic insufficiency</p>

A

<p>fat malabsorption -> steatorrhea</p>

228
Q

<p>chronic inflammatory disease that causes ulceration of the colonic mucosa (most common in rectum and sigmoid colon)</p>

A

<p>ulcerative colitis (UC)</p>

229
Q

<p>idiopathic inflammatory disorder that affects any part of the GI tract from the mouth to the anus; spreads with discontinuous transmural involvement (skip lesions)</p>

A

<p>Crohn's disease (CD)</p>

230
Q

<p>most common sites of CD</p>

A

<p>ascending colon and transverse colon</p>

231
Q

<p>common complications of obesity</p>

A

<p>- cardiovascular problems (HTN, CAD, stroke, MI)- pulmonary (sleep apnea, asthma)- endocrine (NIDDM, infertility)- MSK (OA, low back pain, plantar fasciitis)- GI (GERD, gallstones, fatty liver)</p>

232
Q

<p>portal HTN commonly causes what?</p>

A

<p>- esophageal varices- splenomegaly - caput medusae (ABD varices)- hemorrhoidal varices (internal hemorrhoids)</p>

233
Q

<p>Mechanisms that cause ascites</p>

A

<p>- portal HTN -> increased lymph production -> leakage into peritoneal space and decreased plasma volume- hepatocyte failure -> decreased albumin synthesis -> decreased oncotic pressure in capillaries - altered metabolism + decreased renal flow -> increased RAAS</p>

234
Q

<p>most hazardous toxin not removed from liver during hepatic ecephalopathy</p>

A

<p>- ammonia (end product to protein digestion) -> usually converted to urea</p>

235
Q

<p>causes of hyperbilirubinemia</p>

A

<p>- post hepatic obstruction to bile flow- intrahepatic obstruction- prehepatic excessive production of unconjugated biluribn (hemolysis of RBC)</p>

236
Q

<p>clinical manifestations of cirrhosis</p>

A

<p>- portal HTN (ascites, varices, splenomegaly)- decreased bilirubin metabolism (jaundice)- decreased bile in GI tract (light colored stools)- decreased vitamin K absorption (bleeding)- decreased hormone metabolism and increased androgens/estrogens- decreased protein, fat, and carb metabolism- toxin accumulation (hepatic encephalopathy)</p>

237
Q

<p>lab changes seen with cirrhosis</p>

A

<p>- increased AST and ALT- increased bilirubin- low serum albumin- prolonged PT- elevated alkaline phosphatase</p>

238
Q

<p>5 types of hepatitis and their routes</p>

A

<p>- Hep A (fecal-oral; most common), parenteral, sexual- Hep B (parenteral, sexual, transplacental)- Hep C (parenteral, sexual, transplacental)- Hep D (Hep B coinfection, fecal-oral, sexual)- Hep E (fecal-oral)</p>

239
Q

<p>types of hepatitis that cause chronic active hepatitis</p>

A

<p>- Hep B- Hep B/Hep D coinfeciton- Hep C</p>

240
Q

<p>cardinal manifestations of cholelithiasis</p>

A

<p>- epigastric and right hypochrondrium pain- intolerance of fatty foods</p>

241
Q

<p>pathophysiology of acute pancreatitis</p>

A

<p>- duct obstruction -> acing cell injury- intracellular and extracellular activation of enzymes- lipase -> fat necrosis - trypsin, chymotrypsin, phospholipase, and elastase along w/ inflammation (complement and cytokines) cause cell injury, edema, thrombosis, hemorrhage, and necrosis</p>

242
Q

<p>What can acute pancreatitis lead to?</p>

A

<p>- shock- SIRS- ARDS- acute tubular necrosis (ATN)- coagulation disorders- translocation of intestinal bacteria -> sepsis- pancreatic abscess</p>

243
Q

<p>closely associated w/ development of colorectal cancer</p>

A

<p>colorectal polyps</p>

244
Q

<p>signs and symptoms of colorectal cancer</p>

A

<p>- pain- mass- change in bowel habits- blood in stool- anemia</p>

245
Q

<p>3 criteria for PCOS</p>

A

<p>- few or anovulatory menstrual cycles- elevated levels of androgens- polycystic ovaries (do not have to be present)</p>

246
Q

<p>leading cause of infertility in the US</p>

A

<p>PCOS</p>

247
Q

<p>syndrome directly related to genetic predisposition, insulin resistance, and excess of insulin and androgens</p>

A

<p>PCOS</p>

248
Q

<p>how does insulin resistance and hyperinsulinemia lead to PCOS</p>

A

<p>- insulin resistance overstimulates androgen secretion and reduces hepatic secretion of sex hormone binding globulin- increased free testosterone levels- leads to disordered LH/FSH release- anovulation and hyperandrogenism -> PCOS</p>

249
Q

<p>Why are HTN, dyslipidemia, and hyperinsulinemia commonly present w/ PCOS?</p>

A

<p>- insulin resistance -> more insulin production- high insulin levels -> increased triglycerides and BP</p>

250
Q

<p>clinical manifestations of PCOS</p>

A

<p>- amenorrhea or dysfunctional uterine bleeding- infertility- hirsutism (abnormal hairiness)- acne- HTN- dyslipidemia</p>

251
Q

<p>Most common causes of PID?</p>

A

<p>- gonorrhea- chlamydia</p>

252
Q

<p>complications associated w/ PID</p>

A

<p>- infertility- ectopic pregnancy- pelvic pain and dyspareunia- pelvic adhesions- perihepatitis- ovary and fallopian tube abscess</p>

253
Q

<p>Risk factors for pelvic organ prolapse?</p>

A

<p>- direct trauma (ex. childbirth)- heavy lifting- aging- obesity- hysterectomy</p>

254
Q

<p>descent of a portion of the posterior bladder wall and trigone into the vaginal canal; usually caused by childbirth</p>

A

<p>cystocele</p>

255
Q

<p>bulging of the rectum and posterior vaginal wall into the vaginal canal</p>

A

<p>rectocele</p>

256
Q

<p>Treatment for pelvic relaxation disorders</p>

A

<p>- pessary (for uterine prolapse)- Kegel exercies- surgery</p>

257
Q

<p>benign tumors that develop from smooth muscle cells in the myometrium (often in the fundus); can cause ABD pressure and cramping</p>

A

<p>leiomyoma (aka myoma or uterine fibroids)</p>

258
Q

<p>presence of functioning endometrial tissue or implants outside the uterus (usually ABD and pelvic area); will still respond to hormone fluctuations and can bleed</p>

A

<p>endometriosis</p>

259
Q

<p>clinical manifestations of endometriosis</p>

A

<p>- dysmenorrhea- ABD/pelvic pain- dyspareunia- constipation- infertility</p>

260
Q

<p>list 9 risk factors for breast cancer</p>

A

<p>- increasing age- family hx- genetic predisposition (BRCA 1/2)- early menarche/late menopause- no full-term pregnancies- obesity- sedentary lifestyle- smoking/alcohol- oral contraceptive use or HRT</p>

261
Q

<p>breast cancer manifestations</p>

A

<p>- painless lump on breast- dimpling of skin- edema- orange peel appearance- nipple discharge</p>

262
Q

<p>group of proliferations limited to breast ducts and lobules without invasion of the basement membrane</p>

A

<p>ductal carcinoma in situ (DCIS)</p>

263
Q

<p>Risk factors for male breast cancer</p>

A

<p>- gynecomastia- chest wall irradiation- FHx of Kleinfelters Syndrome- presence of BRCA1 and BRCA 2 mutation- Obesity- Hx of testicular cancer</p>

264
Q

<p>clinical manifestations of ovarian cancer</p>

A

<p>GI symptoms usually first: bloating, flatulence, discomfort</p>

265
Q

<p>most significant risk factor for ovarian cancer</p>

A

<p>family history of ovarian or breast cancer</p>

266
Q

<p>cell surface antigen used to monitor effectiveness of therapy in ovarian cancer if pre-op levels are high; not a good screening tool</p>

A

<p>CA-125</p>

267
Q

<p>diagnostic test for ovarian cancer</p>

A

<p>transvaginal US</p>

268
Q

<p>risk factors for endometrial cancer</p>

A

<p>- obesity- nulliparity- late menopause- HTN- high fat diet</p>

269
Q

<p>most common symptom of endometrial cancer</p>

A

<p>unusual vaginal bleeding</p>

270
Q

<p>clinical manifestations of cervical cancer</p>

A

<p>- may be asymptomatic- vaginal bleeding or discharge</p>

271
Q

<p>clinical manifestations of prostate cancer</p>

A

<p>- signs of bladder outlet obstruction (slow urinary stream, hesitancy, incomplete emptying, frequency, nocturia, and dysuria)- progressive and don't remit (unlike BPH)</p>

272
Q

<p>screening for prostate cancer</p>

A

<p>- digital rectal exam (DRE)- prostate specific antigen (PSA) -> many false positives</p>

273
Q

<p>4 risk factors for testicular cancer</p>

A

<p>- abnormal testicle development- family or personal hx of testicular cancer- hx of undescended testicles- Klinefelter syndrome</p>

274
Q

<p>clinical manifestations of testicular cancer</p>

A

<p>- discomfort or pain in the testicle- feeling of scrotal heaviness- dull ache in lower back or ABD- enlargement of a testicle or change in how it feels- lump or swelling in either testicle</p>

275
Q

<p>condition in which the foreskin cannot be retracted back over the glans</p>

A

<p>phimosis</p>

276
Q

<p>condition in which the foreskin cannot be moved forward (reduced) to cover the glans</p>

A

<p>paraphimosis</p>

277
Q

<p>inflammation of the glans penis; associated w/ poor hygiene and phimosis</p>

A

<p>balanitis</p>

278
Q

<p>abnormal dilation of the testicular vein and pampinoform plexus within the scrotum; described as a "bag of worms"</p>

A

<p>varicocele</p>

279
Q

<p>group of abnormalities in which the testis fails to descend completely</p>

A

<p>cryptorchidism</p>

280
Q

<p>clinical manifestations of BPH</p>

A

<p>- urgency- delay in starting urination- decreased force of stream- long-term urinary retention</p>

281
Q

<p>overdevelopment of breast tissue in males</p>

A

<p>gynecomastia</p>

282
Q

<p>causes of gynecomastia</p>

A

<p>imbalance of estrogen/testosterone due to- hypogonadism- Klinefelter syndrome- testicular neoplasms- drugs</p>

283
Q

<p>3 bacterial STIs</p>

A

<p>- gonorrhea- chlamydia- syphilis</p>

284
Q

<p>2 parasite STIs</p>

A

<p>- scabies/crabs</p>

285
Q

<p>1 fungal STI</p>

A

<p>candida albicans</p>

286
Q

<p>2 viral STIs</p>

A

<p>- HPV- genital herpes</p>

287
Q

<p>2 protozoan STIs</p>

A

<p>- trichamonisasis (trich)- giardia lamblia (giardiasis)</p>

288
Q

<p>common causes of anemia</p>

A

<p>- impaired erythrocyte production - blood loss (acute or chronic) - increased erythrocyte destruction - combo of these 3 factors</p>

289
Q

<p>4 common symptoms of anemia (due to tissue hypoxia)</p>

A

<p>- weakness/fatigue- pallor (skin and mucous membranes)- dyspnea on exertion and increased RR- dizziness and syncope</p>

290
Q

<p>cardiac and renal compensatory mechanisms for anemia</p>

A

<p>Cardiac:</p>

<p>- tachycardia - increased stroke volume - capillary dilation</p>

<p>Renal</p>

<p>- RAAS - increased salt and H2O retention - increased extracellular fluid</p>

291
Q

<p>anemias characterized by erythrocytes that are unusually large in size, thickness, and volume; normal Hgb (normocrhomic)</p>

A

<p>macrocytic (megaloblastic) anemia</p>

292
Q

<p>anemias that result due to ineffective erythrocyte DNA synthesis -> due to vitamin B12 or folate deficiencies</p>

A

<p>macrocytic (megaloblastic) anemia</p>

293
Q

<p>most common type of macrocytic anemia and is caused by vitamin B12 deficiency</p>

A

<p>pernicious anemia (PA)</p>

294
Q

<p>symptoms of pernicious anemia</p>

A

<p>- weakness/fatigue- paresthesias in feet and fingers (neuro manifestations from B12 deficiency)- difficulty walking- loss of appetite/weight loss- sore tongue that is smooth and beefy red</p>

295
Q

<p>manifestations specific to folate deficiency anemia</p>

A

<p>- cheilosis (scales/fissures in mouth)- stomatitis (inflammation of mouth)- burning mouth syndrome (painful ulcers in buccal mucosa and tongue)- GI problems: dysphagia, flatulence, and watery diarrhea</p>

296
Q

<p>anemias characterized by abnormally small erythrocytes that contain abnormally reduced amounts of Hgb</p>

A

<p>microcytic-hypochromic anemias</p>

297
Q

<p>2 types of microcytic-hypochromic anemias</p>

A

<p>- iron-deficiency anemia (IDA)- sideroblastic anemias (SA)</p>

298
Q

<p>2 causes of IDA</p>

A

<p>- inadequate dietary intake- chronic blood loss</p>

299
Q

<p>clinical manifestations of IDA</p>

A

<p>- typical anemia symptoms- nails become brittle and "spoon-shaped"- tongue papillae atrophy (soreness/redness/burning)- gastritis- neuromuscular changes (numbness/tingling)- irritability and headache</p>

300
Q

<p>lab findings for IDA</p>

A

<p>- decreased iron levels- increased total iron binding capacity (TIBC) - transferrin is empty</p>

301
Q

<p>heterogenous group of inherited or acquired disorders characterized by anemia of varying severity and presence of ringed sideroblasts in bone marrow</p>

A

<p>sideroblastic anemias (SAs)</p>

302
Q

<p>clinical manifestations of SAs</p>

A

<p>- CV and respiratory manifestations- hemochromatosis (iron overload)- mild-moderate hepatosplenomegaly- bronze-tinted skin may occur</p>

303
Q

<p>anemias characterized by erythrocytes that are relatively normal in size and Hgb content but insufficient in number</p>

A

<p>normocytic-normochromic anemias (NNAs)</p>

304
Q

<p>5 types of normocytic-normochromic anemias</p>

A

<p>- aplastic - posthemorrhagic- acquired hemolytic- hereditary hemolytic- anemia of chronic inflammation</p>

305
Q

<p>anemia due to damage to bone marrow erythropoiesis (bone marrow failure)</p>

A

<p>aplastic anemia</p>

306
Q

<p>stem cell disorder w/ hyperplastic and neoplastic BM alterations that causes uncontrolled proliferation of RBCs (normally due to JAK2 mutation)</p>

A

<p>polycythemia vera (PV) or primary polycythemia</p>

307
Q

<p>clinical manifestations of PV</p>

A

<p>- unique feature: aquagenic pruritus (painful itching when exposed to heat or water)- red color in face, hands, feet, ears, and mucous membranes- engorgement of retinal and cerebral veins -> cerebral thrombosis likely- HA, delirium, mania, psychotic depression, chorea, visual disturbances</p>

308
Q

<p>common AR disorder of iron metabolism and is characterized by increased GI iron absorption and tissue deposition</p>

A

<p>hereditary hemochromatosis (HH)</p>

309
Q

<p>lab findings of HH?</p>

A

<p>- elevations in serum iron levels and ferritin levels (iron in hepatocytes)- decreased TIBC (transferrin is saturated)</p>

310
Q

<p>benign, acute, self-limiting, lymphoproliferative syndrome characterized by acute infection of B cells and usually transmitted through saliva; most commonly caused by EBV</p>

A

<p>infectious mononucleosis (IM)</p>

311
Q

<p>classic symptoms of infectious mononucleosis</p>

A

<p>- pharyngitis- lymphadenopathy- fever- fatigue (may last 1-2 months after infection)- splenomegaly may occur</p>

312
Q

<p>aggressive, fast growing leukemia with too many lymphoblasts (immature WBC) found in the blood and BM</p>

A

<p>acute lymphocytic leukemia (ALL)</p>

313
Q

<p>aggressive, fast growing leukemia w/ too many myeloblasts (immature WBC that are not lymphoblasts) found in the blood and BM</p>

A

<p>acute myelogenous leukemia (AML)</p>

314
Q

<p>leukemia most commonly seen in children</p>

A

<p>ALL</p>

315
Q

<p>most common adult leukemia</p>

A

<p>AML</p>

316
Q

<p>lymphoid progenitors</p>

A

<p>B cells and T cells</p>

317
Q

<p>myeloid progenitors</p>

A

<p>- basophils- eosinophils- neutrophils- monocytes- erythrocytes- platelets</p>

318
Q

<p>common clinical manifestations of leukemia</p>

A

<p>- anemia -> fatigue- bleeding -> skin, gums, MM, GI tract, petechiae, ecchymosis - infection -> fever- weight loss/anorexia- bone pain- liver, spleen, and lymph node enlargement- elevated uric acid levels</p>

319
Q

<p>slowly progressing disease w/ too many blood cells (not lymphocytes) made in the BM</p>

A

<p>chronic myelogenous leukemia (CML)</p>

320
Q

<p>slow-growing cancer in which too many immature lymphocytes are found mostly in the blood and BM</p>

A

<p>chronic lymphocytic leukemia (CLL)</p>

321
Q

<p>leukemia caused by BCR-ABL fusion gene derived from reciprocal translocation of chromosomes 9 and 22 (Philadelphia chromosome)</p>

A

<p>CML</p>

322
Q

<p>most common clinical finding in patients w/ CLL</p>

A

<p>lymphadenopathy (most are asymptomatic)</p>

323
Q

<p>3 phases of CML</p>

A

<p>- chronic phase (asymptomatic)- accelerated phase (primary sxs develop)- termal blast phase (blast crisis) -> survival of 3-6 monthslater stages resemble acute leukemia but w/ more prominent and painful splenomegaly</p>

324
Q

<p>malignant lymphoma that progresses from one group of lymph nodes to another, including systemic symptoms and presence of B cells called Reed-Sternberg (RS); peripheral nodes (cervical, axillary, inguinal)</p>

A

<p>Hodgkin lymphoma</p>

325
Q

<p>progressive clonal expansion of B cells, T cells, or NK cells (mostly B cells);localized to single axial group of nodes</p>

A

<p>Non-Hodgkin lymphomas</p>

326
Q

<p>fast-growing B cell tumor that is more common is Africa</p>

A

<p>Burkitt lymphoma</p>

327
Q

<p>symptoms of B cell lymphomas (HL, NHL, can be seen in LL)</p>

A

<p>- fever- night sweats- weight loss</p>

328
Q

<p>plasma cell (B cell) cancer characterized by slow proliferation of malignant cells w/ tumor cell masses in the BM usually resulting in destruction of the bone</p>

A

<p>multiple myeloma (MM)</p>

329
Q

<p>common presentation of MM</p>

A

<p>- hypercalcemia- renal failure -> secondary to hypercalcemia and Bence Jones proteins- anemia- bone lesions- Bence Jones protein in urine (Ig fragments formed by bone lesions)</p>

330
Q

<p>platelet count less than 150,000 platelets/uL</p>

A

<p>thrombocytopenia</p>

331
Q

<p>immune mediated, adverse drug reaction caused by IgG antibodies against heparin-platelet factor 4 complex -> platelet activation -> platelet consumption</p>

A

<p>heparin-induced thrombocytopenia (HIT)</p>

332
Q

<p>although the hallmark of HIT is thrombocytopenia, what else are patients at risk for?</p>

A

<p>thrombosis due to activation, aggregation, and consumption of platelets</p>

333
Q

<p>most common cause of thrombocytopenia secondary to increased platelet destruction; usually secondary to infections or other conditions that cause large amounts of antigen in the blood -> immune complex w/ platelets -> destruction</p>

A

<p>immune thrombocytopenic purpura (ITP)</p>

334
Q

<p>multisystem disorder (defect of ADAMS 13) characterized by thrombotic microangiopathy (TMA) -> platelets aggregate and cause occlusion of arterioles and capillaries within microcirculation -> increased platelet consumption and tissue ischemia</p>

A

<p>thrombotic thrombocytopenic purpura (TTP)</p>

335
Q

<p>symptoms of TTP (5)</p>

A

<p>- extreme thrombocytopenia (<20,000)- intravascular hemolytic anemia- ischemic signs and symptoms (most often in CNS)- kidney failure- fever</p>

336
Q

<p>acquired clinical syndrome characterized by widespread activation of coagulation resulting in formation of fibrin clots in microvasculature throughout body</p>

A

<p>disseminated intravascular coagulation (DIC)</p>

337
Q

<p>causes of DIC (5)</p>

A

<p>- trauma- sepsis- cancer- products of conception- injury to endothelium</p>

338
Q

<p>explain how DIC causes clots</p>

A

<p>massive activation of clotting cascade -> widespread microvascular thrombosis and vascular occlusion -> ischemic tissue damage</p>

339
Q

<p>explain how DIC causes bleeding</p>

A

<p>- widespread thrombosis causes consumption of platelets and clotting factors- also causes activation of plasmin and fibrinolysis (try to break up clots) -> lysis of clotting factors and inhibition of platelet aggregationOVERALL: platelets and clotting factors all used up from clots but even if they were available -> clotting system would inhibit further clots from forming to stop potential bleeding</p>

340
Q

<p>clinical manifestations of DIC</p>

A

<p>- oozing from puncture sites- GI bleeding- weakness/fatigue- cyanosis/hypoxiemia- hematuria/oliguria/renal failure</p>

341
Q

<p>elevated fibrin degradation products (FDP) and D-dimer are hallmark findings of what?</p>

A

<p>DIC</p>

342
Q

<p>EBV is linked to which lymphoma</p>

A

<p>Burkett's lymphoma</p>

343
Q

<p>most treatable version of lymphoma</p>

A

<p>Hodgkin's lymphoma</p>

344
Q

<p>elevated reticulocyte count</p>

A

<p>hemolytic anemia</p>

345
Q

<p>group of bone marrow failure disorders where blood cells in BM don't mature; precursor to leukemia</p>

A

<p>myelodysplastic disorder (MDS)</p>

346
Q

<p>Tx for sickle cell crisis</p>

A

<p>- pain control- O2- rehydrate (dehydration major cause)</p>

347
Q

<p>Normal hematocrit (Hct) level</p>

A

<p>38-54%</p>

348
Q

<p>Normal hemoglobin (Hgb) level</p>

A

<p>11.7-14.9 g/dL (lower end in females)</p>

349
Q

<p>Normal RBC level</p>

A

<p>4.2-6.1 million cells/mcL</p>

350
Q

<p>Normal WBC count</p>

A

<p>5,000-10,000</p>

351
Q

<p>immature form of neutrophils; elevated in blood during infection (high production from BM)</p>

A

<p>bands</p>

352
Q

<p>very early and immature form of WBC; sign of leukemia when increased numbers found on blood smear</p>

A

<p>blast cells</p>

353
Q

<p>normal platelet (Plt) count</p>

A

<p>150,000-300,000</p>

354
Q

<p>measure of the extrinsic clotting pathway</p>

A

<p>prothrombin time (PT)</p>

355
Q

<p>Normal PT range</p>

A

<p>10-13 seconds</p>

356
Q

<p>common cause of prolonged PT</p>

A

<p>Coumadin therapy</p>

357
Q

<p>measure of the intrinsic clotting pathway</p>

A

<p>partial thromboplastin time (PTT)</p>

358
Q

<p>Normal PTT range</p>

A

<p>30-45 seconds (other references say 25-35 seconds)</p>

359
Q

<p>common causes of prolonged PTT</p>

A

<p>Heparin therapyHemophilia</p>

Pathophysiology (20 decks)

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