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MM: Histology > IntroPathologySSN > Flashcards

IntroPathologySSN Flashcards

1
Q

Postmitotic

A

heart, nerve. Replaced by scar when injured

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2
Q

intermitotic

A

divide all the time. Rapid turnover. Intestine, epithelial, skin, bone marrow

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3
Q

reverting mitotic

A

usually don’t divide but can when injured. Hepatocytes, renal tubular eptothelium

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4
Q

lipofuscin

A

old age/wear-and-tear pgment in liver and heart

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5
Q

free radical injury

A

physical, radiation: breaks chromosomes, diarrhea, hair loss, low blood count

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6
Q

free radical damage in

A

S and G2, intermitotic cells particularly

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7
Q

types of free radicals

A

lipid peroxidation, protein cross-linking, DNA mutation, superoxide, hydroxyl, peroxide

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8
Q

cytopathic viral infections

A

interfere with cel metabolism

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9
Q

Immune-mediated viral damage

A

against virus or virus-altered cells

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10
Q

cytomegalovirus

A

in immune-supressed pt., cell becomes huge

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11
Q

two ways chemicals damage

A

directly combine with molecule or organelle, or reactive metabolite binds membrane protein or lipid

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12
Q

hypoxia/ischemia

A

lactic acid causes pH drop, causes ATPase disfunction, Na influx, swelling

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13
Q

reversible hypoxia

A

ER swells, mitochondria condense, ribosomes disaggregate, glycogen stores used up.

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14
Q

irreversible hypoxia

A

cell rupture

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15
Q

necrosis triggers

A

neutrophils

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16
Q

test for necrosis with

A

trypan blue binds cells in lab (not diagnostic)

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17
Q

gross necrosis

A

plase area with yellow and hemorrhage Nuclei disappear, incoming neutrophils, hypereosinophilic

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18
Q

caseous necrosis

A

whitelooking areas of necrosis

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19
Q

nuclear breakdown

A

pyknosis (enlarged), karyorrhexis (nucleus breakdown) karyolysis (small bits)

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20
Q

mitochondrial apoptosis

A

release superoxides, mito pores releases cytochrome C, causes caspase 9 and activates DNAases

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21
Q

Death-receptor apoptosis

A

cytoplasmic caspace 8 activation. T-cells bind FAS. Chromatin forms DNA ladders, Blebs form apoptotic bodies

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22
Q

acute inflammation: vascular phase

A

Dolor, rubor, calor, tumor, functio laesa

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23
Q

dolor (pain)

A

fleeting vasoconstriction (seconds); mediated by nerve endings

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24
Q

rubor (red) and calor (heat)

A

progressive vasodilation of arterioles, cap bed and venules increases blood flow

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25
Q

histamine, leukotrienes, bradykinin

A

rela arteriole smooth muscle

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26
Q

tumor and functio laesa

A

increase vascular permeability and hydrostatic pressure; leakage of fluids into interstitial space; edema

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27
Q

transudate

A

low cells, low protein. Duration of leak depends on endothelial injury

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28
Q

exudate

A

transudate after cellular phase. Cell and protein rich

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29
Q

assume neutrophils in exudate unless

A

allergy, drug rxn, parasite (eosinophil), or viral (lymphocyte)

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30
Q

acute inflammation: cellular phase

A

margination, rolling with transient adhesions. Firm adhesion, transmigration

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31
Q

margination

A

vasodilation slows blood flow, nuetrohils migrate to flow periphery

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32
Q

rolling with transient adhesions: P-selectin endothelia

A

histimine, thrombin, sialyl-Lewis X oligosaccharides, LAD-2 disease

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33
Q

rolling with transient adhesions: E-selectin endothelia

A

TNF, IL-1, sialyl-lewis X oligosaccharides, LAD-2 disease

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34
Q

firm adhesion: ICAM-1 endothelia

A

TNF, IL-1, LFA-1 (integrin), LAD-1 disease

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35
Q

firm adhesion: VCAM-1 endothelia

A

TNF, IL-1, VLA-4 (integrin)

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36
Q

transmigration PECAM-1 (CD-31) endothelia

A

collagenases (from neutrophils)

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37
Q

opsinization

A

how antibodies coat patholgens

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38
Q

opsonins

A

help host phagocytotic cells bind and destroy pathogen

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39
Q

TLRs

A

toll like receptors, are pattern recognition receptors that let innate immune cells (neutrophils) bind molecular motifs common to pathogens

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40
Q

PAMPS

A

pathogen associated molecular patterns, what TLRs on neutrophils recognize

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41
Q

neutrophil receptors

A

FcR, CR1, CR3, C1q, TLR4

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42
Q

FcR ligand

A

IgG (opsonin)

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43
Q

CR1, CR3 ligand

A

C3 (opsonin)

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44
Q

C1q ligand

A

Collectins (opsonin)

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45
Q

TLR4 ligand

A

LPS (a PAMP)

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46
Q

steps of opsination and destruction

A
  1. recognition and attachment 2. engulfment 3. phagosome 4. phagolysosome 5. destruction via reactive oxygen species
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47
Q

O2 to Superoxide, hydrogen peroxide, hydroxyl radical: enzymes and location

A

NADPH oxidase, mitochondria

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48
Q

Nitric Oxide (NO) enzyme and location

A

iNOS (+arginine) in cytoplasm

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50
Q

acute inflammation outcomes

A

resolve, abscess, turn to chronic inflammation (hours or days)

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51
Q

fibrinous exudate

A

forms on inflammed organs b/c tissue factos are released, causing extrinsic coagulation cascade

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52
Q

green in pus

A

comes from heme component of MPO

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53
Q

cytokines

A

mediate inflammation and immune response

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54
Q

TNF & IL-1

A

cytokines produced by macrophages that activate the endothelium

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55
Q

chemokines

A

recruit leukocytes (in inflammation states) and organize B and T-cells in the spleen and lymph nodes (in normal tissue)

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56
Q

Chemokine examples

A

**CC (adjacent cysteine residues) and CXC (cysteines separated by another amino acid)

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57
Q

lysosomal enzymes of leukocytes

A

mediate acute inflammation: proteases which act on kininogen and complemet proteins (c3, c5)

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58
Q

neuropeptides

A

small substances initiate inflammatory response

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59
Q

Nitric Oxide (NO) enzyme and location

A

Short-lived soluble free radical gas, causes smooth muscle relaxation and vasodilation

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60
Q

plasma protein derived mediators

A

produced in liver and present in blood inactive. Complement activation ( C3a, C5a, C3b, C5b-9) and factor XII (kinin system)

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61
Q

plasma proteins

A

C1-C9 play role in host defense and inflammation

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62
Q

membrane attack complex

A

C5-C9, degrade membrane for cell lysis

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63
Q

complement activation pathway: classical

A

Ag-Ab complexes; IgG/IgM

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64
Q

complement activation pathway: alternative

A

bacterial polysaccharides

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65
Q

complement activation pathway: lectin

A

binds mannose residues microbes

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66
Q

systemic effects of inflammation: exogenous pyrogens

A

macrophages release TNF and IL-1 ->cyclooxygenase increase, prostaglandin production

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67
Q

systemic effects of inflammation: increase in acute phase proteins

A

liver production of C reactive protein, serum amyloid A, fibronogen

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68
Q

C reactive protein

A

CRP, opsonization

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69
Q

serum amyloid A

A

SAA, opsonization

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70
Q

fibrinogen

A

increases erythrocyte sedimentation rate

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71
Q

systemic effects of inflammation: leukocytosis

A

increase of WBCs from bone marrow

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72
Q

chronic inflammation causes

A

caused by infection or de novo from chronic disease

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73
Q

chronic inflammation involves

A

lymphocytes, plasma cells and macrophages (not neutrophils of acute)

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74
Q

granulomas

A

activated macrophages plus T-cells, eosinophils, around an indigestible antigen or as part of a type IV hypersensitivity response

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75
Q

granulomas lead to

A

chronic scarring/fibrosis/calcification

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76
Q

granuloma serious clinical problems

A

schistosomiasis, sarcoidosis, inflammatory bowel disease

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77
Q

types of granuloma

A

infectious (parasitic, fungal, bacterial), foreign body, unknown, miscellaneous

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78
Q

caseating granulomas

A

necrotizing, as in TB, less clear borders, denucleiated ded cells

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79
Q

noncaseating granulomas

A

as in sarcoidosis, macrophages, giant cells, clear border (surrounded by lymphocytes)

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80
Q

platelets

A

bud off megakarocytes. Replace every 10 days. 6 day shelf life.

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81
Q

platelets cause vasoconstriction

A

by releasing ADP/thromboxane A2 (TxA2)

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82
Q

thrombocytopenia

A

less than 150,000 platelet count, need transfusion

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83
Q

platelet plug formation

A

adhesion, activation, aggregation

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84
Q

vWF (adhesion)

A

Cross-linked dimers bind collagen and platelets

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85
Q

A3 domain

A

where vWF binds collagen exposed at site of injury

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86
Q

Gp1b receptor (A1 domain)

A

where vWF binds platelet

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87
Q

ADAMTS13

A

cleaves vWF multimers at A2 (to minimize clot size

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88
Q

defects in vWF

A

von Willebrand disease: easy bruising, nosebleeds, dental bleeding, menorrhagia

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89
Q

von Willebrand type I

A

low vWF. Most common form

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90
Q

von Willebrand type II

A

AD or AR, may not bind VIII, platelets correctly

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91
Q

vonW type 2M

A

A1 loF mutation. Platelets can’t bind. (GeI=NL; ristocetin=no clumping)

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92
Q

vonW type 2A

A

defects in A2/crosslinking

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93
Q

vonW type 2B

A

A1 GoF (increased A1/Gp1b interaction). Clotting in general circulation, less avail for injury

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94
Q

vonW type 2N

A

poor binding to VIII

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95
Q

von Willebrand type 3

A

AR, no vWF syth so VIII is very low. Rare.

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96
Q

thrombotic thrombocytopenic purpura (TTP)

A

lack of ADAMTS13 leads to spontaneous clotting

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97
Q

5 signs of TTP

A

microangiopathic hemolytic anemia, low platelets, neuro, renal, fever.

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98
Q

TTP affects

A

Young adults, mainly female. High mortality if untreated

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99
Q

Congenital TTP

A

AR, rare, no ADAMTS13. Neonatal jaudice, some present as adults. Give FFP (contains ADAMTS13)

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100
Q

acquired TTP

A

autoimmune, Abs to ADAMTS13. Treat with plasmapheresis

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101
Q

acquired TTP induced by

A

clopidogrel

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102
Q

platelet activation

A

stabilizes adhesion. Platelets spread on top of wound

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103
Q

major platelet activators

A

Thrombin/collagen+TxA2/ADP

104
Q

platelet GpVI

A

binds exposed collagen, transmit IC signals to increase Ca, release TxA2/ADP (promotes aggregation)

105
Q

platelet PAR1

A

binds with thrombin, transmit IC signals to increase Ca, release TxA2/ADP (promotes aggregation)

106
Q

ADP binds

A

P2Y12 receptor on platelets

107
Q

TxA2 binds

A

TxA2 receptor on platelets

108
Q

clopidogrel blocks

A

P2Y12 receptor on platelets

109
Q

ASA blocks

A

TxA2 production

110
Q

Hermansky Pudlak syndrome

A

platelets lack ADP granules. Lower platelet activation, bleeding.

111
Q

integrins

A

transmembrane domains that require conformational change to bind ligand

112
Q

GpIIb/IIIa

A

integrin on platelets essential for aggregation. EC is fibrinogen receptor.

113
Q

GpIIb/IIIa requires activation by

A

ADP/thrombin

114
Q

Glanzmann’s thrombasthenia

A

AR. abnormal GpIIb/IIIa, fibrinogen can’t bind/stabilze clot. Bleeding.

115
Q

aggregation balance between

A

ADP/TxA2 (pro-aggregation, from platelets) & PGI2/NO (anti-thrombotic, from endothelium)

116
Q

Atherosclerosis & clotting

A

damaged endothelium can’t release antithrombic factors easily (low cAMP, high Ca, high platelet activation)

117
Q

primary hemostasis

A

platelet plug

118
Q

secondary hemostatis

A

clotting cascade

119
Q

tertiary hemostasis

A

clot degeneration by plasmin as injury heals

120
Q

fibrin

A

glue that holds platelets together (goal of clotting cascade)

121
Q

clotting system max rate depends on

A

tenase, prothrombinase complexes

122
Q

extrinsic clotting pathway

A

tissue factor (TF) exposed(+VII); Xa(+Va)=prothrombinase; early thrombin (IIa) burst activates intrinsic pathway (via XI, VIII & V)

123
Q

intrinsic clotting pathway

A

XII activates at negatively charged surface; Xia;IXa(+VIIIa)=tenase; Xa

124
Q

common clotting pathway

A

Xa+Va; IIa (thrombin); Ia (fibrin); crosslinked by XIIIa

125
Q

anticoagulants: TFPI

A

inhibits VIIa/TF/Xa complex

126
Q

anticoagulants: ATIII-Heparin

A

inactivates thrombin, Xa, Ixa

127
Q

anticoagulants: Protein C,S, thrombomodulin

A

Cleaves Va, VIIIa

128
Q

anticoagulants: Plasmin

A

cleaves fibrin, V, VIII

129
Q

50% defect of any anti-coagulant

A

increase risk of thrombosis

130
Q

100% defect of any anti-coagulant

A

neonatal purpura fulminans: cutaneous haemorrhage and necrosis, low blood pressure, fever and disseminated intravascular coagulation

131
Q

HIF

A

Hypoxia-inducible factor

132
Q

HIF major effects

A

POG: decrease cell proliferation, increase oxygen delivery, increase glucose metabolism

133
Q

HIF-1

A

heterodimer, expressed by all cells, metabolism and glycolysis

134
Q

HIF-1 alpha subunit

A

constantly made, degraded if O2 is present

135
Q

HIF-1 beta subunit

A

combines with alpha when hypoxic; activation

136
Q

HIF-2

A

oxygen delivery. Expressed by endothelium, lungs, kidney and macrophages

137
Q

HIF-2 acts on

A

EPO, VEGF, transferrin

138
Q

VHL: Von Hippel-Lindau tumor suppressor

A

protein, forms complex that breaks down HIF (by ubiquination).

139
Q

Vin Hippel-Lindau syndrome

A

AD loss of VHL function=more cancers (esp. renal cell carcinoma, pheochromocytoma, hemangioblastoma)

140
Q

chuvash polycythemia

A

AR mutation in VHL=higher HIF expression, overproduction of red cells, increase risk of thrombosis

141
Q

Chuvash and erythropoietin sensitivity

A

HIF is more stable, so EPO is overproduced in kidney=polycythemia. Mutant VHL also can’t inhibit JAK2-STAT5 pathway in erythroid porgentiors=more proliferation in response to erythropoetin

142
Q

Warburg effect

A

cancer cells mostly make energy by lactic acid fermentation even when O2 is present.

143
Q

cause of Warburg effect

A

tumor makes lots of HIF-1, up-regulates LDHA, inactivates PDH

144
Q

upregulated LDHA

A

converts more pyruvate to lactate

145
Q

inactivated PDH

A

shunts pyruvate out of TCA cycle

146
Q

altitude sickness

A

too much hemoglobin increases blood viscosity, which reduces tissue oxygenation

147
Q

Why do Tibetans have normal hemoglobin levels?

A

mutations reduce HIF-2 expression.

148
Q

shock

A

circulatory perfusion insufficient for oxygenation and waste removal

149
Q

3 major types of shock

A

cardiogenic (MI or CHF), hypovolemic (hemorrage or dehydration), redistributive (sepsis, anaphylaxis, toxins, drugs, neurogenic)

150
Q

5 signs of shock

A

CHOMM: cool clammy skin, hypotension, oliguria, mental status, metabolic acidosis

151
Q

cool clammy skin

A

skin vasoconstricts, trying to compensate for hypovolemia

152
Q

hypotension

A

absolute (systolic < 90mmHg) or relative (systolic drop > 40 mmHg)

153
Q

oliguria

A

low urine output because kidneys aren’t being perfused

154
Q

mental status

A

agitation; confusion and delirium; coma

155
Q

metabolic acidosis

A

liver, kidney and muscles not clearing lactic acid

156
Q

3 stages of shock

A

initial, Day 2-6, day 10-14

157
Q

initial shock

A

electrolyte imbalance (from acidosis, low output)

158
Q

Day 2-6 shock

A

renal dysfunction and necrosis, fluid overload, edema, acidosis, uremia, oliguria, may see manifestations of brain damage

159
Q

Day 10-14 shock

A

kidneys heal: diuretic/resolution phase

160
Q

hemorrhage percents

A

15% is mostly tolerable, 40% will kill without aggressive resuscitation

161
Q

hematoma

A

massive clot

162
Q

hemo-[location]

A

blood where blood should not be. (hemopericardium, hemothorax)

163
Q

bleeds into skin

A

petechia<ecchymosis

164
Q

hemorrhage treatment goals

A

restore volume, maintain oxygenation, reverse or prevent coagulopathy, eliminate cause

165
Q

edema

A

transudate (SG 1.020). only exudate is inflammatory

166
Q

virchow traid (thrombosis)

A

endothelial injury, abnormal blood flow, hypercoagulability

167
Q

thrombosis: arterial origin

A

coronary, cerebral, aortic

168
Q

thrombosis: venous origin

A

90%! deep leg, peri-uterine, peri-prostatic

169
Q

thrombosis: mural origin

A

clot forms along wall of damaged heart

170
Q

DIC: disseminated intervascular coagulation

A

small petechia in capillaries. Sepsis, childbirth (amniotic fluid TF in maternal blood), glandular cancers (when TF is produced)

171
Q

DIC diagnosis

A

D-dimer measures breakdown products of fibrin

172
Q

acute inflammation outcomes

A

Minimal necrosis, if stimulus is destroyed. Necrosis is stimulus is not destroyed.

173
Q

minimal necrosis outcomes

A

normal tissue & mild burn if exudate is resolved, scarring & fibrinoprurulent percarditis, peritonitis if exudate is organized

174
Q

necrosis outcomes

A

labile or stable cells, or permanent cells

175
Q

permanent necrotic cells

A

scar from MI

176
Q

labile or stable necrosis

A

framework intact: normal tissue, lobar pneumonia. Framework destroyed: scar, bacterial abscess

177
Q

keloids

A

excessive scar (TIMP unchecked)

178
Q

contractures

A

tightening of skin after burns

179
Q

inadequate scar

A

dehiscence (wound comes apart), ulceration

180
Q

stages of wound healing

A

hemostasis, inflammation, proliferation, remodeling

181
Q

inflammation in wound healing

A

neutrohils and macrophages. After hemostasis (platelets and clotting factors)

182
Q

neutrophils in wound healing

A

arrive first (72 hours), remove debris

183
Q

macrophages in wound healing

A

remove debris, screte cytokines and Gfs that signal angiogenesis and ECM remodeling

184
Q

proliferation

A

3-7 days, remove fibrin clot, angiogenesis (VEGF!), re-epithelialize, matrix deposited (granulation tissue!)

185
Q

remodeling

A

weeks. Collagen remodeling (balance of MMP and TIMP), wound contraction (myofibroblasts)

186
Q

neoplasia

A

new growth

187
Q

anaplasia

A

neoplasm with dedifferentiation. Not good.

188
Q

dysplasia

A

disorderly maturation (HPV-cervix, smoking-lungs, GERD-esophagus)

189
Q

grading

A

looking at cells

190
Q

staging

A

T: where primary tumors are, N: region lymph nodes, M: metastasis

191
Q

-oma

A

benign

192
Q

-sarcoma, -carinoma

A

malignant (exception: invasive meningioma, melanoma)

193
Q

AR diseases of defective DNA repair

A

Xeroderma pigmentosum, ataxia telangiectasia, bloom sydrome, Fanconi anemia

194
Q

xeroderma pigmentosum

A

severe sunburn, discoloring, skin cancers

195
Q

ataxia telangiectasia

A

ataxia, mental development decrease, discolored skin, x-ray sensitivity

196
Q

bloom syndrome

A

short stature and tendency to develop cancers

197
Q

fanconi anemia

A

ashkenazi Jews and afrikaners. Acute myelogenous leukemias, bone marrow failure, and developmental disabilities

198
Q

Stain: CK7+CK20-

A

tracheal cancer

199
Q

Stain: CK7-CK20+

A

colon cancer

200
Q

Stain EGFR

A

lung cancer

201
Q

metastasis dissemination

A

seeding of body cavities (ovarian), lymphatic spread (carinoma), hematogenous spread (sarcoma)

202
Q

metastasis steps: detachment

A

through E-caherin loss

203
Q

metastasis steps: ECM degradation

A

via MMP and TIMP collagenases. Then attach to new ECM

204
Q

metastasis steps: migration

A

cytokine, autocrine, or paracrine stimulated motility

205
Q

metastasis steps: travel as tumor emboli

A

selectin selection, ICAM and VCAM for locale stabilization, then diapedesis and invasion of endothelial cells

206
Q

homing of tumor to certain locales

A

CXCR4, 7 in breast cancer, CDCL12 and CCL21 elsewhere

207
Q

tissue architecture: benign

A

well circumscribed, encapsulated

208
Q

tissue architecture: malignant

A

poorly circumscribed, lack of cell polarity and epithelial connections

209
Q

cytologic features: benign

A

small uniform cells, no visible nucleoli

210
Q

cytologic features: malignant

A

large, pleomorphic, larger hyperchromatic nuclei. Nucleus as big as cytoplasm

211
Q

differentiation: benign

A

well differentiated, resembles cell of origin

212
Q

differentiation: malignant

A

well differentiated if metastasized, otherwise numerous bizarre mitoses

213
Q

rate of growth: benign

A

slow, some dependence on hormones

214
Q

rate of growth: malignant

A

rapid, areas of necrosis from outgrowing blood supply

215
Q

local invasion: benign

A

encapsulation, does not invade

216
Q

local invasion: malignant

A

can invade and destroy adjacent tissue w/MMP, metastasize

217
Q

biomarker: CEA

A

colon cancer

218
Q

biomarker: AFP

A

Hepatoma

219
Q

biomarker PSA

A

prostate cancer

220
Q

biomarker Ca-125

A

Ovarian cancer

221
Q

biomarker CA19-9

A

bile cancer

222
Q

biomarker HCG

A

testis and placenta cancer

223
Q

biomarker calcitonin

A

medullary cancer

224
Q

asbestos causes

A

mesothelioma (cancer of protective lining of organs)

225
Q

benzene causes

A

leukemia, hodgkin lymphoma

226
Q

UV causes

A

Xeroderma pigmentosum

227
Q

Most common cancer incidence

A
  1. breast/prostate 2. lung 3. colon
228
Q

Highest mortality cancer

A
  1. lung 2. breast (F), colon (M) 3. Colon (F), Prostate (M)
229
Q

cancer symptoms

A

TNF, Paraneoplastic syndrome, trousseau phenomenon

230
Q

TNF & IL-1

A

Cachexia, suppresses fatty acid metabolism, catabolism

231
Q

paraneoplastic syndrome

A

ectopic hormones (PTH-rP-hypercalcemia, ADH waterlogging)

232
Q

trousseau phenomenon

A

miniclots all over the body

233
Q

Making Cancer

A
  1. self-sufficient growth signals 2. insensitivity to anti-growth factors 3. tissue invasion/metastasis 4. limtless replication potential 5. sustained angiogenesis 6. evading apoptosis
234
Q

Self-sufficient growth factors: glioblastoma

A

PDGF/PDGFR

235
Q

Self-sufficient growth factors: sarcoma

A

TGFalpha/TGFalphaR

236
Q

SS receptor: squamous cell lung cancer

A

increased ERBB1 (EGFR)

237
Q

SS receptor: breast cancer

A

increased Her2/ERBB2

238
Q

2nd messengers: neurofibromatosis

A

RAS GTPase (inactivating) is mutated. Leads to elephant man

239
Q

2nd messenger: ACR-ABL kinase

A

chromosome translocation leads to uninhibited tyrosine kinase

240
Q

limitless replication

A

overexpression of telomerase , overrides p53/RB checkpoints

241
Q

HPV16, 18

A

carcinoma of cervix

242
Q

HHV8 virus

A

kaposi sarcoma

243
Q

HBV, HCV virus

A

hepatocellular carcinoma

244
Q

EBV virus

A

B-cell and nasopharyngeal cancer

245
Q

nonlethal damage to cancer?

A

Proto-oncogenes, tumor suppressors, apoptosis related, DNA repair genes

246
Q

rolling: selectins

induced by

A

histimine, thrombin, TNF and IL-1

247
Q

adhesion: integrins

pairing

A

IFA to ICAMS

VFA to VCAMS

248
Q

FcR and complement bind what why?

A

IgG, C3, collectins

to opsonize antigen!

249
Q

LAD 1

A

adhesion defect (LFA)

250
Q

LAD 2

A 
rolling defect
(P selectin)
251
Q

chronic granulomatous disease

A

NADPH oxidase deficient

252
Q

Chediak-Higashi

A

can’t deliver bacteria to lysosomes

253
Q

high in cell

A

K, glucose, negative charge

254
Q

low in high

A

Na, Cl-

MM: Histology (6 decks)

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