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Block 1 > Path 2 > Flashcards

Path 2 Flashcards

1
Q

homeostasis vs adaptation

A

steady state where intracellular milieu = WNR of physiologic parameters vs adjustment in structure and fxn to accommodate changing demands and extracellular stresses (reversible)

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2
Q

4 types of cellular adaptations: hyperplasia vs hypertrophy vs atrophy vs metaplasia

A

inc # of cells, can have same size and appearance as nml counterparts, REVERSIBLE vs inc structural proteins and organelles proportionally –> inc size of organ/tissue; often in cells w/ limited cap to divide; can occur w/ hyperplasia vs dec in size and # of cell, SOMETIMES REVERSIBLE vs change in morphology and acquisition of new features –> 1 differentiated cell type = replaced by another differentiated cell type; adoptive response to chronic irritation/stimulus. REVERSIBLE. does not cross germ layers (ie. bone doesn’t become nervous tissue, connective tissue doesn’t become epithelial tissue). can lead to malignant epithelial tumors

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3
Q

3 multiplication categories of hyperplasia

A

labile cells - all lining epithelia cont to multiply throughout life; stable cells - parenchymal cells of all glandular organs (liver, kidn, pancreas) and smooth muscle that can multiply but nmlly quiescent; permanent cells - neuron, myocardial cells, skel muscle cells can’t multiply

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4
Q

3 types of hyperplasia

A

physiologic: triggered by hormone lvls –> temporary change in organ’s fxnal state; once hormone dec –> cells = nml size; ex: breast and uterus. compensatory: triggered by loss of cells/tissue –> cells grow to compensate for loss of fxn; ex: partial hepatectomy, unilateral nephrectomy. pathologic - triggered by excessive hormonal or growth factor stimulation; abnl but controlled; hyperplasia = not ca but can lead to ca; ex: gynecomastia post estrogen therapy for prostatic ca, endometrial hyperplasia (from continuous estrogen prod unopposed by progesterone, could be endo/exogenous), BPH

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5
Q

hypertrophy and examples

A

inc structural proteins and organelles –> inc size of organ/tissue; often in cells w/ limited cap to divide; can occur w/ hyperplasia

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6
Q

3 types of hypertrophy

A

physiologic: triggered by inc in fxnal demand; ex: skel muscle in bodybuilders. compensatory: triggered by loss of part of tissue, hypertrophy and hyperplasia caan coexist; ex: partial hepatectomy, unilateral nephrectomy. pathologic: triggered by inc work in organ; ex: cardiac muscle in arterial HTN, smooth muscle of bladder in BPH

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7
Q

2 types of atrophy

A

physiologic: impt for fetal and natal growth and adult life; ex: regression of thyroglossal duct during fetal development. pathologic: triggered by dec workload like fx (disuse atrophy), diminished blood flow (vascular atrophy), loss of innervation like paralysis (denervation atrophy), old age (senile atrophy), starvation like malnutrition, loss of endocrine stimulation, pressure like hydronephrosis; ex: involution of thymus in adult maturation, bone atrophy (localized = disuse osteoporosis, generalized = postmenopausal osteoporosis)

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8
Q

2 mechanisms of atrophy

A
  1. cell deletion like apop. 2. cell shrinkage like autophagocytosis (self eating) and ubiquitin pathway (proteasomes)
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9
Q

2 types of metaplasia

A

epithelial: columnar to sq, ex: bronchial sq metaplasia from smoking; sq to columnar, ex: glandular metaplasia of Barrett’s esophagus. connective tissue metaplasia, ex: bone metaplasia in atherosclerotic lesion, myositis ossificans (bone formation in muscle)

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10
Q

intracellular accumulation

A

manifestation of metabl derangements; happens in cyto, organelles, nucleus –> can be harmless or toxic

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11
Q

ex of lipid accumulation

A

TAG accumulate in hepatocytes –> form 1 large droplet not bound by membrane; chol accumulate in macs => foam cells –> atherosclerotic plaques

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12
Q

how are fats seen under microscope?

A

oil red O, Sudan III, Sudan IV, Sudan black –> fat soluble; you see empty holes b/c TGs = lost during paraffin processing

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13
Q

steatosis

A

in liver, myocardium, kidney, muscle; toxins like CCl3 poisoning, Amanita phalloides poisoning, alc, protein malnutrition/inhibit synthesis, anoxia, DM, obesity –> abnormal accumulation of TGs and/or free fatty acids (FFAs) in parenchymal cells

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14
Q

if TG = white, why is steatosis yellow?

A

b/c buildup of carotenoids (lipochromes) dissolved in the droplets

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15
Q

steatosis in myocardium

A

aka lipomatosis, adipositas cardis; from prolonged moderate to severe hypoxia –> Lipid droplets in myocardial fibers

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16
Q

acute vs chronic alc effects

A

inc NADH/NAD+ ratio (for q ETOH –> you make NADH) –> inhibits TCA –> FA catabolism to acetyl CoA –> excess acetyl CoA –> ketone bodies –> ketogenesis –> ketoacidosis; inc NADH –> inhibits FA [O] –> FA synthesis –> TAG –> VLDL –> hyperlipidemia; inc NADH –> pyru to lactate –> inhibits gluconeogenesis –> lactic acidosis, hypoglycemia; inc NADH –> inhibits glycolysis –> hyperglycemia; inc NADH –> inhibits protein synthesis. REVERSIBLE EFFECTS vs alc-induced liver dz, alc-induced hepatitis, hepatic steatosis aka fatty liver, cirrhosis, inc acetald and free radicals. IRREVERSIBLE EFFECTS

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17
Q

steatosis from hypoxia

A

hypoxia –> dec RBC –> anemia –> less FFA [O] for energy –> FFA remain in cyto for TG synthesis

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18
Q

Micronutrient (vitamin-mineral) malnutrition vs Protein energy malnutrition

A

Marasmus - inadequate intake of protein and calories,
Kwashiorkor - normal calorie intake with inadequate protein intake

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19
Q

steatosis from starvation

A

Hepatomegaly and steatosis
• Lipoproteins not made
• Liver cells cannot export their TGs
Hypoalbuminemia
• Inadequate protein synthesis in liver
Abdomen appears swollen
• (a) ascites (from increased peritoneal fluid hypoalbuminemia)
• (b) hepatomegaly (from steatosis)

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20
Q

how is chol removed?

A

in liver; Esterified and stored in membrane bound droplets, Transfer to HDL –> transported to the liver –> excreted in bile

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21
Q

how do atherosclerotic plaques form?

A

minor dmg to blood vessel wall –> macs = recruited and uptake LDLs –> macs = filled w/ lipids => foam cells –> foam cells accumulate –> plaques rupture –> clot forms –> cells take up more LDL –> fat builds up –> fibroblasts excrete fibrous proteins –> cells die and leave debris –> more macs recruited –> cycle rpts until blood vessel = blocked

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22
Q

xanthomas vs xanthelasmas

A

Yellow tumorlike lumps of foam cells from complication of hypercholesterolemia; in subepithelial connective
tissue of skin and tendons; Acquired or hereditary vs little yellow lumps that develop on the eyelid or at the nasal corner of the eye

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23
Q

Period acid-Schiff (PAS)

A

periodic acid oxidizes glucose residues and creates aldehydes that react with the Schiff reagent and creates a purple-magenta color
• Stains structures with a high proportion of carbohydrate macromolecules
• Mucus, basal membrane, fungal walls

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24
Q

glycogen storage dz (GSD)

A

hereditary deficiency of one of the enzymes
involved in the degradation of glycogen –> increased intracellular glycogen storage

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25
Q

lipofuscin accumulation

A

yellow-brown, finely granular cytoplasmic,
often perinuclear pigment; seen in permanent cells like neurons, metabolic cells like liver, brown atrophy (brownish color of atrophic organs, involves intensive autophagy)

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26
Q

melanin accumulation

A

Brown black dermal pigment formed
by enzyme tyrosinase; Catalyzes oxidation of tyrosine to
dihydroxyphenylalanine in melanocyte

27
Q

Ferritin and Hemosiderin

A

iron storage (free iron = toxic –> must be bound to ferritin or hemosiderin; 20% of the total iron stored as hemosiderin and ferritin in liver, spleen, and bone marrow

28
Q

Ferritin and Hemosiderin accumulation

A

iron overload –> tissue hemorrhage/bruise; systemic overload –> Hereditary hemochromatosis: control of intestinal absorption of dietary iron is lost –> deposition of hemosiderin, hemosiderosis: Repeated blood transfusions –> similar conseq to Hereditary hemochromatosis

29
Q

bilirubin accumulation

A

end product of heme degradation.
• breakdown of senescent red cells by spleen liver and marrow
• When bilirubin accumulates systemically and deposits in tissues –> yellow discoloration of jaundice (icterus)

30
Q

calcification

A

deposition of calcium salts in the wrong place; common and benign; calcium phosphate precipitates any time there is a shift to alkalinity and dissolves in acid pH

31
Q

2 types of calcification: dystrophic vs metastatic

A

Calcium phosphate deposits locally in dying tissues; Necrotic areas (coagulative, caseous, liquefactive); Plasma levels of calcium and phosphate are nml; usually a tell tale sign of previous injury vs Calcium phosphate deposits occur body-wide in otherwise normal tissues; Plasma levels of calcium are elevated (hypercalcemia); law of Askanazy: calcium metastases favor organs that lose acid –> have an internal alkaline compartment

32
Q

ex of dystrophic vs metastatic calcification

A

calcification of aortic valve, lithopedion/stone baby vs stomach: “grating under knife”, lungs: “bathing sponge” b/c alveoli = stiff from Ca2+, kidney: calcification of the tubular epithelium, tubular basement membranes and
interstitium => nephrocalcosis, nephrolithiasis

33
Q

edema vs hyperemia vs hemorrhage vs thrombosis vs embolism vs infarction

A

water moving from vascular wall to interstitial space d/t vascular permeability vs inc vol of blood in vessel of tissue vs extravasation of blood d/t vessel rupture or dzed vascular wall; inc blood vol outside of vessel vs blood clotting at inappropriate sites, attach to wall vs migration of blood clots carried by blood to distant site and obstruct blood flow vs developing necrosis in area distal to obstruction of end-artery

34
Q

4 types of edema: transudate vs exudate vs lymphedema vs myxedema

A

protein poor (<3g/dL), pitting edema vs protein rich (>3g/dL), no pitting edema (inc hydrostatic pressure/dec oncotic pressure) vs protein rich, no pitting edema vs protein rich, no pitting edema; lymphatic system = dmged or blocked –> buildup of interstitial fluid (ex: filariasis by W. bancrofti, lymphogranuloma venereum - edema in inguinal region by chlamydia STD) vs accumulation of glycosaminoglycans –> attract water –> no pitting edema; from hypo/hyperthyroid

35
Q

edema = excess extracellular fluid. ECF = divided into 2 subcompartments; which ions/molec in each compartment?

A

blood plasma and interstitial fluid. Na+ and glu in ECF, K+ in ICF

36
Q

relationship b/w hydrostatic vs oncotic pressure. what’s oncotic pressure?

A

they’re opposites: high hydrostatic pressure/low oncotic pressure at arterial end, low hydrostatic pressure/high oncotic pressure at venule end (b/c there’s high protein –> attracts more H2O –> more oncotic pressure). osmotic pressure induced by albumin; ex: malnutrition w/ low protein intake –> Kwashiorkor, cirrhosis w/ dec albumin synthesis, nephrotic syndrome w/ inc loss of protein in urine, protein-losing enteropathies

37
Q

ex of pitting edema

A

DVT in LE, pulm edema in L sided heart failure, peripheral pitting edema in R sided heart failure, portal HTN in liver cirrhosis producing ascites

38
Q

local vs generalized edema

A

inflamm edema, venous obstruction, lymphatic destruction vs cardiogenic edema, nephrogenic edema, edema assoc w/ liver cirrhosis

39
Q

generalized cardiogenic edema: backward failure vs forward failure

A

infarct of L ventricle –> blood backs up in lungs –> pulm edema –> L side failure; R side failure –> generalized edema in subq tissues. ex: swelling of ankles and feet in walking pts (b/c fluid builds up there), swelling in lower back if pt is bedridden, rapid wt gain d/t fluid retention –> all R side failure; dyspnea and cough producing pink frothy sputum –> pulm edema vs dec cardiac output –> reduced renal perfusion –> reduced renal blood flow –> dec glomular filtration –> kidney secretes renin –> renin/angiotensin/aldosterone axis kicks in to secrete more aldosterone –> sodium retention –> inc intravascular vol and improved cardiac output, but extra fluid causes inc venous pressure and edema

40
Q

generalized nephrogenic edema

A

by glomerular mechanism: glomeruli = leaky –> albumin lost from plasma to urine –> reduce plasma oncotic pressure
by renin: adrenals secrete aldosterone to inc sodium reabsorption –> retained sodium expands blood vol –> edema
by failing to secrete sodium and H2O: daily vol of urine prod dec to minimum –> fluid intake inc –> blood vol inc –> edema

41
Q

generalized liver cirrhosis

A

roots of portal vein= strangled –> backup of portal blood flow –> insufficient albumin prod in liver –> aldosterone = inactivated

42
Q

hyperemia vs congestion

A

lots of blood supply in an organ d/t inc fxnal demands –> active process vs lots of venous stagnant blood d/t impaired outflow from tissue –> passive process, can be systemic (global cardiac failure) or local (isolated venous obstruction), bluish/purple like cyanosis so not bright red

43
Q

chronic liver congestion

A

caused by heart failure; effects of chronic congestion on structure and fxn of liver; dec R ventricle –> venous pressure move to liver via IVC and hepatic veins –> venous congestion impedes efficient sinusoidal blood flow in terminal hepatic venules –> sinusoidal stasis –> accumulation of deO2 blood in centrilobular areas –> liver cirrhosis, collagen deposition, fibrosis

44
Q

chronic pulm congestion

A

caused by L side heart failure on structure and fxn of lung, can be acute (dyspnea, cough w/ pink frothy sputum) or chronic (cough w/ rusty-colored sputum)

45
Q

internal hemorrhage: hematoma vs hemothorax vs hemopericardium vs hemoperitoneum vs hemarthrosis

A

accumulation of blood w/ soft tissues vs hemorrhage in pleural cavity vs hemorrhage in pericardial cavity vs hemorrhage in peritoneal cavity vs hemorrhage in synovial cavity

46
Q

hematuria vs hematemesis vs melena vs hematochesia vs hemptysiss vs menorrhagia vs metrorrhagia

A

blood in urine –> kidney or urinary tract dz vs blood in vomit –> esophageal or gastric hemorrhage vs bloody stool –> upper GI bleeding, blood = partially digested by HCl and turns black => hematein vs blood thru rectum –> large intestine dz vs blood from lungs vs heavy menstrual bleed vs irreg menstrual bleed

47
Q

thrombosis

A

formtion of thrombus (solid intravascular mass that ATTACHES to vessel wall and forms during life and from constituents of blood, contains PLT/fibrin/entrapped cellular contents)

48
Q

red vs white vs mixed thrombi

A

venous thrombi, more RBCs, form slowly vs arterial thrombi, PLTs and fibrin/less RBCs vs in heart or aorta, red alternates w/ white (red w/ RBC, white w/ plts and fibrin) => lines of Zahn

49
Q

mural thrombi vs occluding thrombi vs valvular thrombi vs canalized thrombi vs saddle thrombus vs septic thrombi

A

attached to vessel or heart wall and restricts lumen vs fill lumen completely vs attach to heart valves, aka vegetations vs occur when new blood channels form in an organized thrombus vs straddle the bifurcation of blood vessels (mostly pulm arteries) vs contain bacteria

50
Q

3 factors that predispose to thrombosis

A

Virchow’s triad: endothelial cell injury, alteration in blood flow, hypercoagulable state

51
Q

endothelial cell injury vs alteration in blood flow vs hypercoagulable state

A

trauma –> endothelial die and slough off –> subendothelial collagen exposed –> circulating plts contact exposed collagen and undergo aggregation –> thrombosis vs slowing of blood flow –> plts and clotting factors have more time to stick –> thrombosis (ex: DVT, immobilization from bone fx, prolonged bedrest, obese or pregnant individuals); high laminar flow –> turbulent flow –> thrombosis (ex: varicose veins, vascular aneurysms) vs any alterations in coagulation => thrombotic diathesis; inherited like mutations in factor V gene or prothrombin gene, homocystinuria, defic in anticoagulants like antithrombin III/protein C/protein S or acquired; acquired like prolonged bedrest, ocp, pregnancy, disseminated ca, heparin-induced thrombocytopenia syndrome, antiphospholipid ab syndrome

52
Q

fates of thrombus

A
  1. growth from mural to occluding
  2. propagation: thrombus inc in size and extend along venous segment in direction of circulation
  3. dissolution/lysis: thrombus dissolved by fibrinolytic activity of blood
  4. embolization: thrombus breaks off and become embolus
  5. organization: thrombus = invaded by cellular elements from vein wall –> thrombus firmly attaches to vein wall where this occurs
  6. fibrosis: end stage of organization of thrombus, collagen matures and capillary network regresses
  7. recanalization: end stage of organization of thrombus, new blood vessels grow w/in thrombus
53
Q

venous thrombi vs arterial thrombi

A

vs

54
Q

embolism

A

solid, liq, gas objects carried by blood and large enough to impact downstream lumen –> complete vascular occlusion, ischemic necrosis of distal tissue; impaction can be from peripheral veins and end in lungs => pulm thromboembolism, or from arterial blood and end in arteries => systemic thromboembolism

55
Q

pulm thromboembolism vs systemic thromboembolism

A

thrombus from deep veins from thigh or popliteal vein blocks pulm artery –> asx if small; pleuritic chest pain, pleural effusion, hemoptysis; sudden death; chronic PE w/ numerous asx emboli in small pulm arteries vs LE –> limb/foot/toe gangrene, brain via middle cerebral artery –> stroke or TIA, small bowel via superior mesenteric artery –> bowel infarction, spleen and kidney –> small renal or splenic infarcts, UE –> limb/hand/finger gangrene

56
Q

paradoxical thromboembolism

A

made in systemic veins, bypass lungs, and end up in systemic arteries; large emboli bypass by going thru ventricular septal defect or patent formamen ovale (R to L passage in heart); small emboli bypass thru arteriovenous anastomoses in pulm circ; rare

57
Q

fat embolism

A

fat tissue passes into bloodstream, stop in lungs, squeeze thru alveolar capillaries or travel thru arteriovenous shunts, enter systemic circ, and lodges w/in blood vessel from trauma, parenteral lipid infusion, pancreatitis, burns, childbirth

58
Q

clinical signs of fat embolism

A

tachypnea, tachycardia, confusion/stupor/coma, reddish-brown nonpalpable petechiae rash –> pathognomonic sign

59
Q

mechanical theory vs biochemical theory of fat embolism

A

from mechanical obstruction of pulm and systemic vasculature w/ embolized fat vs non toxic TGs = degraded in plasma into FFA which are toxic to pneumocyte and lung capillaries –> alveolar hemorrhage and edema –> neu = activated –> acute respiratory distress syndrome (ARDS)

60
Q

gas embolism

A

gas bubbles in circ obstructing vascular flow and causing distal ischemic injury; d/t iatrogenic gas embolism like catheters or procedures, chest/neck trauma, decompression sickness (DCS/Caisson dz) like scuba diving

61
Q

type I vs type II DCS. how to tx?

A

mild; pain in joints of UE or LE => “bends”; from presence of bubbles in periarticular tissue vs severe; affect ears (vertigo, N/V), lungs (cough, chest pain, SOB), spinal cord (paraplegia, tetraplegia, incontinence), brain (HA, confusion, double vision). tx: recompression then slow decompression

62
Q

amniotic fluid embolism

A

amniotic fluid w/ fetal cells/debris in maternal circ d/t tear in placental membrane –> anaphylaxis, histamine release, igE

63
Q

infarction. white vs red infarcts

A

area of ischemic necrosis d/t occlusion of arterial supply or venous drainage. ischemic/anemic/pale infarcts; in organs w/ end-arterial circ (no anastomoses connecting terminal arteries to e/o); ex: heart, spleen, kidney, brain, retina vs hemorrhagic infarct; in tissues w/ dual blood supply; ex: lungs –> low bp in pulm arteries, high bp in bronchial arteries –> if pulm artery = occluded, bronchial circ has to save it or else infarcted

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