Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Goljan Path > Cell Injury > Flashcards

Cell Injury Flashcards

1
Q

Oxygen Content

A

= Hgb x O2Sat + PaO2; Oxygen in RBC attached to Heme group is Oxygen SATuration (PULSE Oximeter). PaO2 = oxygen dissolved in plasma. If ppO2 dec, O2Sat has to decrease b/c heme gets oxygen from blood.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Ischemia

A

Decrease in arterial blood flow (e.g. thrombus, cardiogenic shock)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Hypoxia vs. Hypoxemia

A

Hypoxemia is a cause of hypoxia. Hypoxemia is low partial pressure of oxygen in arterial plasma. Dalton’s law…O2, Co2, N (remains constant). Retains Co2 (Any RESP acidosis) —> PaO2 MUST go down (Dalton’s). ANY resp acidosis -> hypoxemia.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Respiratory distress syndrome

A

Ventilation defect. Hyaline membrane disease. No ventilation but perfusion = intrapulmonary shunt. Patient with hypoxemia, gave 100% O2 but PO2 DIDN’T INCREASE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Perfusion defects

A

Dead space defect. e.g. PE. 100% O2 will help!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Diffusion defect

A

e.g. Fibrosis (sarcoidosis), pulmonary edema

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Hypoxia 2/2 by hgb related problems

A

Anemia - PaO2 NORMAL, so OXSat normal, but HGB decreases. CO - heater in winter-time, auto exhaust, house-fire, high affinity for hgb—> meaning that O2Sat DECREASES. Tx = 100% O2. Cyanide (polyurethane products in house fire!).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Methemoglobinemia

A

Hb w/ Fe3+. “Chocolate covered blood.” PaO2, Hgb normal. But OxygenSat NOT. Still cyanotic after 100%. NItrates/nitrites in mountains oxidize hgb –> Fe3+ (mountain guy comes down w/ cyanosis). IV METHYLENE BLUE. Vitamin C (reducing agent) is side. Dapsone (treated for leprosy) = sulfa drug. Sulfa and Nitro drugs produce methhemoglobin + could produce G6PD hemolytic. Common in HIV b/c of ppx for PCP w/ TMP-SMX.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What will right shift HgB?

A

2,3-BPG, fever, low pH, high altitude (respiratory alkalosis, hyperventilate). Lower oxygen affinity = good!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Left shift hgb?

A

Hb F, CO, methhemoglobin, high pH; can’t release O2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Cytochrome oxidase - last enzyme before Oxygen acceptor

A

3 C’s - cytochrome oxidase, cyanide, co; all inhibit cytochrome oxidase.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Uncoupling

A

When intramembrane is permeable to H+. Dinitrophenol (preserving wood), alcohol, salicyclates. Increased NADH and FADH2, temperature increases. Hyperthermia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Anaerobic glycolysis used for tissue hypoxia

A

End product is lactate. Every cell can do. Surviving on 2 ATP per glucose with tissue hypoxia. Build-up of lactic acid in cell and outside. (Inc. AG-graph metabolic acidosis).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Inc acid in cell

A

Denature structures and enzymes. COAGULATION necrosis. Can’t even apoptosis itself.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

W/o ATP, all ATPase pumps problem

A

Na/K (digoxin). Na+ gets into the cell –> water inside –> cellular swelling. Reversible.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Calcium in tissue hypoxia

A

It enter cells. Ca-ATPase pump generally keeps it out. ATP decreased, Ca+ has easy access. Activates phospholipases (membrane dog), nuclear pyknosis, mitochondria. Irreversible change. CELL membrane damage.

17
Q

Free radicals

A

Lipofuscin is an end-product. Lipids are not digestible all the way = lipofuscin. Free radical has unpaired e- in outer orbit = unstable. Retinopathy of prematurity, bronchopulmonary. H2O -> OH-. Ionizing radiation produces hydroxyl free radicals -> mutations (leukemia is most common). Fe makes hydroxyl free radicals.

18
Q

Acetaminophen

A

Free radical damage to liver (and kidney). Occurs right around CENTRAL vein b/c farthest away from hepatic artery. Tx = N-acetylcysteine —> replenishes glutathione. Fulminant liver disease. Damages renal medulla. (ASA gets rid of PGE2 - vasodilator - leaves A-II in charge –> vasoconstriction + renal medulla w/ free radicals –> renal tubules —> renal papilla).

19
Q

Superoxide free radical neutralizer

A

Superoxide mutase (SOD)

20
Q

Glutathione

A

Pentose phosphate shunt. F(x) = neutralizes free radicals, esp. drug and any peroxide ones.

21
Q

Carbon tetrachloride

A

Dry cleaning industry –> free radical (liver). CCl3 -> fulminant liver failure.

22
Q

Apoptosis

A

Embryology - lumens for solid organs, MIF (uterus, cervix, upper 1/3 vagina). Caspases —> apoptotic bodies to be phagocytosed. Lipofuscin is left-over. Women (Wollfian duct structure - epididymis, seminal vesicles, vas deferens). Thymic involution. Cancer-killing. Atrophy (reduced tissue mass). Liver w/ hepatitis - Councilman body, red neuron.

23
Q

Coagulation necrosis

A

Pale on gross. Pale vs. hemorrhaghic infarct. Good consistency = pale (heart, kidney, spleen ok, liver…). Hemorrhagic - GI, testicle, lung. Vague outlines of normal tissue.

24
Q

Dry gangrene

A

NO PUS. e.g. Diabetic. Popliteal artery.

25
Q

Bowel infarction

A

Most common is adhesions from pervious surgery. Second is incarcerated in inguinal hernia.

26
Q

Only place where infarction does NOT lead to coagulation necrosis

A

CNS - liquefactive necrosis. Brain has little structure –> liquify. NETUROPHILS. MOST of the time, liquefactive is actually an infectious picture.

27
Q

Coagulase -> coagulation (Fibrin) strands –> ABSCESS

A

Strep releases hydrouranidase breaks down surrounding tissues -> cellulitis

28
Q

Caseous necrosis

A

Systemic fungal or mycoplasma; The lipid of the cell wall –> Cheesy appearance. Caseation is ONLY for fungal or mycobacterial. Granuloma-type necrosis can also be sarcoid, etc.

29
Q

Pancreas is retroperitoneal

A

Therefore pain gets referred to the pain (epigastric -> refer to back)

30
Q

Fatty necrosis

A

Enzymatic fat necrosis. Also in breasts - but that’s traumatic (calcify) - and PAINFUL while cancer is usually not painful. Enzymatic fat necrosis is UNIQUE to the pancreas. FA + Ca -> chalky areas.

31
Q

Calcium stains blue on H&E

A

Dystrophic calcification. Like atherosclerotic plaque.

32
Q

Fibrinoid necrosis

A

Necrosis of IMMUNOLOGIC disease. IC-deposition.

33
Q

Palpable purpura

A

T-III, small vessel disease. IC deposition in small vessel, glomerulus. Activates complement (alternative) –> C5a –> chemotactic factor for Neutrophils. Neutrophils ACTUALLY do the damage.

34
Q

Sinusoids vs fenestrated epithelium

A

RBCs go through vs. filtration (e.g. kidney)

35
Q

Fatty change

A

EtOh is most common cause. Acetyl-CoA and NADH required in EtOH metabolism. Alcoholics always have lactic acidosis b/c increase in NADH —> drive pyruvate to lactate. In fasting state, alcoholic won’t be able to gluconeogenesis –> fasting hypoglycemia. Increased synthesis w/ acetyl-CoA with beta-hydroxybutyric acid high. Ketoacidosis.

36
Q

Fatty change pathogenesis

A

Glycerol-3-P shuttle. Also carbohydrate backbone for TG’s. VLDL in liver (endogenous production from glycolysis -> G3P -> TG’s).

Goljan Path (9 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions