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Step 1 Prep > Pathology > Flashcards

Pathology Flashcards

1
Q

The exception to the rule that pathologic hyperplasia can lead to dysplasia cancer.

A

BPH: benign prostatic hyperplasia

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2
Q

Major cellular mechanism of cellular hypertrophy

A

Protein synthesis, gene activation and production of organelles (cytoskeleton, mitochondria)

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3
Q

Permnent tissues cannot undergo hyperplasia or hypertrophy. What are the 3 examples of permanent tissue in the body?

A

Hyperplasia

  1. Cardiac muscle
  2. Skeletal muscle
  3. Nerve
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4
Q

Classical example of pathologic hyperplasia leading to dysplasia and cancer (female)

A

Endometrial hyperplasia

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5
Q

Mechanism of atrophy (2)

A
  1. Apoptosis (decrease number of cells)

2. Ubiqiquitin-proteasome degradation of cytoskeleton; autophagy (cell size)

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6
Q

Metaplasia most often involves what body surfaces

A

Surface epithelium

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7
Q

Classical example of metaplasia (GIT)

A

Barret’s esophagus (squamous–> columnar w/ goblet cells)

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8
Q

What is the mechanism of metaplasia? Is it reversible?

A

Reprogramming of stem cells; yes

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9
Q

What is the exception to the rule that metaplasia can progress to dysplasia and cancer (female).

A

Apocrine metaplasia (Fibrocystic change of the breast)

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10
Q

Deficiency of what vitamin can lead to metaplasia, i.e. keratomalacia?

A

Vitamin A: keratomalacia

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11
Q

t(15, 17) translocation

A

APML (cells trapped in blast)

* Treatment with ATRA

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12
Q

Mesenchymal tissues can undergo metaplasia. The classical example is:

A

Myositis ossificans; caused by trauma
(Metaplastic production of bone in the skeletal muscle); look for ossificatiion within the skeletal muscle. This is not an osteosarcoma b/c there is distinct separation

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13
Q

How do you differentiate between osteosarcoma and myositis ossificans on an X-ray?

A

OS: part of bone
MO: distinct separation of bone from muscle

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14
Q

3 uses of vitamin A in the body

A
  1. Night blindness
  2. Immuno cells
  3. Specialized epithelium
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15
Q

T/F Dysplasia is reversible

A

True

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16
Q

Aplasia; classical example

A

Failure of cellular production during embryogenesis

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17
Q

Hypoplasia; classical example

A

Decrease in cell production during embryogenesis

Streak ovary in Turner Syndrome

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18
Q

Cell injury occurs when stress ___________

A

Exceeds a cell’s ability to adapt; type of stress, severity, type of cell affected

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19
Q

Slow progressive decrease in blood supply to the kidney results in _________; whereas a rapid decrease in blood supply results in _______

A
  1. Atrophy

2. Infarction

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20
Q

T/F Neurons are very susceptible to hypoxia.

A

True

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21
Q

Common causes of cellular injury

A

Inflammation, nutritional deficiency/excess, hypoxia, trauma, genetic mutations

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22
Q

Define hypoxia

A

Low oxygen delivery to tissue; low ATP; cellular injury

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23
Q

The 3 major causes of hypoxia

A
  1. Ischemia
  2. Hypoxemia
  3. Decreased O2 carrying capacity of the blood
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24
Q

Define ischemia. Through what 3 mechanisms can ischemia occur?

A

Decreased blood flow through an organ;

  1. Arterial flow blockage (atherosclerosis)
  2. venous outflow obstruction
  3. Shock (heart, hypovolemic, neurogenic, septic, anaphylactic)
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25
Q

What is Budd Chiari syndrome? What is the most common cause of Budd Chiari syndrome?

A

Thrombosis of the hepatic vein

* Polycythemia vera (most common cause of Budd Chiari)

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26
Q

What AI disorder is associated with Budd Chiari Syndrome?

A

SLE; lupus anti-coagulant

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27
Q

Define hypoxemia.

A

Low partial pressure of O2 in the blood ( PaO2< 60; < 90%)

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28
Q

Describe the sequence of events in oxygenation of the blood.

A

FiO2 –> PAO2 –> PaO2 –> SaO2
FiO2: high altitude
PAO2: CO2 build up, PAO2 goes down
PaO2: i/s fibrosis lung

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29
Q

Decreased O2 carrying capacity arises with Hb loss or dysfunction. Give several examples.

A
  1. Anemia: decrease RBC mass; PaO2 and SaO2 are normal
  2. CO poisoning [binds Hb 100X > O2]
  3. Methemoglobinemia
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30
Q

In CO poisoning, is PaO2 normal? Is SaO2 normal?

A 
PaO2 = normal
SaO2 = decreased
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31
Q

Exposures to CO

A

Fires, exhaust from cars, gas heaters

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32
Q

The classic sign of CO poisoning clinically. The first detectable symptom of CO poisoning – good for screening.

A

Sign: Cherry red appearance of the skin
Symptom: headache

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33
Q

Heme contains Fe2+ iron. Fe3+ cannot bind O2. Metheoglobinemia is seen clinically under these circumstances

A

Oxidant stress: sulfa drugs, nitrate drugs, newborns

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34
Q

Classic clinical finding in methemoglobinemia. Treatment is:

A

Chocolate-colored blood with cyanosis

Treatment: IV methylene blue which will reduce iron back to 2+ state

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35
Q

Hypoxia impairs oxidative phosphorylation. The key consequences is that this results in…

A

Decreased ATP

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36
Q

Low ATP disrupts 3 key cellular functions. Name them.

A
  1. Na-K pump [cell swelling]
  2. Ca pump [high IC Ca can activate enzymes = bad]
  3. Aerobic glycolysis [lactic acid can denature DNA and proteins]
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37
Q

The initial phase of cellular injury is reversible. What is the hallmark sign of reversible cell injury?

A

Cellular swelling; leads to loss of microvilli [like blowing up a glove], membrane blebbing [cytoskeleton pulled away from cell membrane] and swelling of RER [ribosomes pop off / decreased protein synthesis]

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38
Q

Reversible or irreversible cell injury: Loss of microvilli, membrane blebbing and swelling of RER (which leads to ribsome detachement and dereased protein synthesis)

A

Reversible cell injury

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39
Q

Hallmark of irreversible cell damage. The 3 membranes affected.

A

Cell membrane damage

  1. Plasma membrane (enzyme in blood, IC Ca increases)
  2. Mitochondrial membrane
  3. Lysosome
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40
Q

Where is the ETC? Inner or outer mitochondrial membrane?

A

The inner mitochondrial membrane

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41
Q

Within the mitochondria, cyotchrome c is present. If it leaks into the cytosol, it can activate…

A

Apoptosis

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42
Q

Why is high IC calcium dangerous?

A

It is an enzyme activator

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43
Q

Morphologic hallmark of cell death is…

A

Loss of nucleus; occurs via pynknosis, karyorrhexis, karyolysis

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44
Q

Pynknosis

A

Shink of nucleus (ink dot)

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45
Q

Karyorrhexis

A

Nucleus breaking up into big pieces

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46
Q

Karyolysis

A

Nucleus pieces broken into building blocks

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47
Q

The 2 mechanisms of cell death

A
  1. Necrosis (murder)

2. Apoptosis (suicide)

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48
Q

Necrosis is death of a large group of cells followed by…

A

Acute inflammation

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49
Q

T/F Necrosis is always pathologic

A

True

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50
Q

Coagulative necrosis

A

Necrotic tissue that remains firm; cell shape and organ structure are preserved by coagulation of cellular proteins
* Nucleus disappears; characteristic of all infarction except brain

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51
Q

What is the gross shape of a coagulative necrotic tissue?

A

Wedge-shaped and pale infarct; wedge points to the occlusion

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52
Q

What is red infarction?

A

Blood re-enters a loosely organized tissue. Classic example: testicle.

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53
Q

Liquefactive necrosis (3 examples)

A

Enzymatic lysis of cells and proteins
* Brain (microglial with hydrolytic enzymes), abscess (neutrophils with hydrolytic enzymes), pancreatitis (surrounding = fat necrosis)

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54
Q

Why do we see liquefactive necrosis in the brain?

A

Because the microglial cells have hydrolytic enzymes.

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55
Q

Gangrenous necrosis is…

A

Coagulative necrosis (ischemia of lower limb)

  • Wet gangrene: superimposed infection (Liquefactive)
  • Dry gangrene: mummified tissue
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56
Q

Caseous necrosis

A

Soft, friable necrotic tissue with cottage cheese like appearance. Combination of C & L necrosis; TB/fungal infection (granulomatous)

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57
Q

Fat necrosis (2 classic examples)

A

Chalky white appearance (chalky white appearance due to deposition of calcium); peripancreatic fat & trauma to the breast [giant cells, fat and calcification / can present as a mass]

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58
Q

Saponification

A

Fatty acids released by trauma or lipase join with calcium = dystrophic calcification

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59
Q

Dystrophic calcification

A

Calcium deposition on dead/dying tissue (serum Ca and PO4 normal); psammoma bodies (tumor cells outgrow blood supply)

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60
Q

Metastatic calcification

A

Serum Ca or PO4 elevated and has ability to force Ca into tissue and can precipitate

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61
Q

Fibrinoid necrosis. 2 examples

A

Necrotic damage to BV wall; leaking of proteins into blood vessel wall; results in bright pink staining. Characteristic of malignant hypertension or vasculitis.

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62
Q

In what circumstance would a 30 year old woman present with fibrinoid necrosis?

A

Pre-eclampsia (3rd trimester)

* Fibrinoid necrosis of the placental blood vessels

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63
Q

T/F Apoptosis is energy-dependent, genetically programmed cell death. Three classical examples.

A

True

Ex./ endometrium, embryogenesis (syndactly), killing of virally infected cells by CD8 T cells

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64
Q

Apoptotic bodies that fall from cells are removed by…

A

Macrophages

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65
Q

Apoptosis is mediated by caspases. These caspases activate 2 enzymes

A
  1. Protease (break down cytoskeleton)

2. Endonucleases (break down DNA)

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66
Q

The 3 pathways by which caspases are activated.

A
  1. Intrinsic mitochondrial (cellular injury, DNA damage, decreased hormonal stimulation) –> cytochrome c leaks and activates caspases
  2. Extrinsic receptor-lignad (FAS –> CD95 or death receptor) – TNF-TNFR [best example/ NEGATIVE SELECTION of T cells]
  3. CD8 T-cell pathyway (MHCI –> perforins; granzyme enters pores and activates caspases)
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67
Q

BCL-2’s role

A

Stabilize the mitochondrial membrane so that cytochrome c does not leak out

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68
Q

Oxygen with 1 e, 2 e, 3 e, 4 e. Which is the most damaging?

A
  1. Superoxide
  2. Peroxide
  3. Hydroxide (Most damaging)
  4. Water
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69
Q

Pathologic generation of free radicals

A

Ionizing radiation (OH), inflammation (PMN’s O2 dept mechanism with burst – NADPH oxidase), metals (copper and iron), drugs (acetaminophen, carbon tetrachloride)

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70
Q

What enzyme converts oxygen into superoxide in the respiratory burst?

A

NADPH oxidase

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71
Q

H2O2 is converted by ________ to water.

A

Myeloperoxidase

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72
Q

The fentin reaction generates…

A

The hydroxyl free radical

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73
Q

Underlying mechanism of damage in hemochromatosis or Wilson’s disease?

A

Tissue damage 2/2 free radical damage

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74
Q

Free radicals cause this type of damage to a cell

A
  1. Lipid peroxidation (membrane)

2. Oxidize DNA and proteins (oncogenesis)

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75
Q

Elimination of free radicals (3 mechanisms)

A
  1. Antioxidants (Vitamin A, C, E)
  2. Enzymes (SOD, glutathione peroxidase, catalase)
  3. Metal carrier proteins (Cu/cerruloplasmin and Fe/transferrin+ferritin)
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76
Q

Name each enzyme responsible for detoxifying: superoxide, hydrogen peroxide, hydroxyl radical?

A
  1. SO dismutase
  2. Catalase
  3. Glutathione peroxidase
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77
Q

Describe free radical injury: CCl4 [dry cleaning] and reperfusion injury

A

CCl4 –> CCl3 [P450] damages hepatocytes & fatty liver (inability to synthesize apolipoproteins that excrete fat)

  • Re-perfusion injury: blood returns with oxygen and PMN’s leads to continued injury
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78
Q

Misfolded protein that deposits in EC space, often around blood vessels. What is this protein called?

A

Amyloid

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79
Q

Congo red stain with apple-green birefringence under polarized light.

A

Amyloid

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80
Q

Systemic amyloidosis: primary and secondary

A

Primary: AL (derived from Ig light chain); associated with plasma cell dyscrasia

Secondary: AA (derived from SAA protein – an acute phase reactant); chronic inflammatory states; malignancy; Familial Mediterranean fever

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81
Q

Familial Mediterranean fever

A

AR dysfunction of neutrophils; high SAA acute phase reactant during acute attacks deposits as AA amyloid; presents with episodes of fever and acute serosal inflammation (MI, appendicitis)

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82
Q

Amyloid classical clinical findings

A

Kidney = #1: nephrotic syndrome

  • Restrictive CM/arrhythmia
  • Tongue enlargement, malabsorption, HSM
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83
Q

Senile cardiac amyloidosis; what type of amyloid? Symptomatic?

A

ASYMPTOMATIC (25% patients > 80 years old); Non-mutated serum transthyretin deposits in the heart

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84
Q

Familial amyloid cardiomypoathy

A

Mutated serum transthyretin (5% AA) –> restrictive cardiomyopathy

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85
Q

DM2 amyloidosis

A

Amylin –> pancreas islets (derived from insulin)

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86
Q

Alzheimer’s amyloid plaques made up of

A

B-myloid precursor protein (a-beta); Chromosome 21 [Down’s Syndrome]

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87
Q

Dialysis associated amyloidosis; what type of amyloid?

A

Beta-2 microglobulin [component of Ig] deposits in joints; Builds up in blood

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88
Q

MTC amyloidosis

A

C-cell tumor (calcitonin)

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89
Q

An abscess will have this form of necrosis

A

Liquefactive

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90
Q

Progeria results from a defect in this protein

A

Lamin

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91
Q

Wermer syndrome is similar to Progeria, but patients live into their 50’s. The protein defect in these patients is:

A

Helicase

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92
Q

Lipofuscin deposition in aging cells is 2/2

A

Peroxidation of membrane liquids

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93
Q

What type of cells have the greatest amount of telomerase activity?

A

Germ cells

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94
Q

T/F Metastatic calcification can result from ESRD.

A

True

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95
Q

T/F During pregnancy, the myometrium undergoes smooth muscle hypertrophy

A

True

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96
Q

Mallory body vs. Councilman body

A

Mallory body: Intracytoplasmic intermediate filaments within hepatocytes
Councilman body: Extracytoplasmic; apoptosis of a hepatocyte

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97
Q

Define inflammation

A

Allow PMN’s & Lymphocytes & proteins into tissue space in response to infection

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98
Q

Acute inflammation is characterized by: (2 things)

A

Edema and PMN’s

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99
Q

Acute inflammation arises in response to (2 events)

A

Infection or tissue necrosis

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100
Q

Examples of innate responses

A

Epithelium, mucus, complement, mast cells, macrophages, neutrophils, eosinophils, basophils

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101
Q

Acute inflammation is mediated by several factors.

A
  1. TLR’s
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102
Q

TLR’s are present on macrophages and dendritic cells. They recognize ____________.

A

PAMPS (pathogen associated molecular patterns)

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103
Q

CD__ is present on macrophages and recognizes LPS on outer membrane of GN bacteria

A

CD14

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104
Q

TLR activation results in upregulation of: _______

A

NF-kappa B; molecular on-switch which turns on acute inflammatory response

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105
Q

Arachidonic acid is released from the cell membrane by….

A

PLA2

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106
Q

PGI, D, E mediate vasodilation and increased vascular permeability. Where along the blood vessels do these events occur?

A

Vasodilation (arteriole) increased vascular permeability (post-capillary venule)

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107
Q

PGE2 mediates…

A

Feeeeever and pain

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108
Q

LTB4

A

Attracts and activates PMN’s

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109
Q

LTC, D, E

A

Mediate vasoconstriction, broncospasm, increased vascular permeability

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110
Q

4 key mediators influencing neutrophil chemotaxis

A

LTB4, C5a, IL-8, bacterial products

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111
Q

What is a pericyte?

A

Contains contractile elements underneath endothelial cells. Think leukotrienes.

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112
Q

Where are mast cells? How are they activated (3 methods)?

A

C/T

  1. Tissue trauma
  2. C3a, C5a
  3. Cross-linking IgE by antigen
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113
Q

Histamine granules mediate (2 functions)

A

Vasodilation, increased vascular permeability

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114
Q

The delayed response of acute inflammation involves…

A

Leukotrienes (AA metabolites)

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115
Q

Classical complement

A

C1 to IgG or IgM bound to Ag

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116
Q

Alternative complemenet

A

Microbial products directly activate complement

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117
Q

Mannose-binding lectin pathway

A

MBL binds mannose on microorganisms and activates complement

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118
Q

Result of activation of complement

A

C3 –> C5 convertase –> MAC

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119
Q

C3a & C5a
C5a
C3b
MAC

A

C3a & C5a: Mast cell degran
C5a: chemotactic for neutrophils
C3b: opsonin
MAC: lyses microbes by creating holes in cell membrane

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120
Q

Hageman factor (Factor 12)

A

Activated upon exposure to subendothelial or tissue collagen; also activated in DIC

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121
Q

Hageman factor activates (3)

A
  1. Coagulation
  2. Complement
  3. Cleaves HMWK to bradykinin [similar to histamine + pain]
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122
Q

2 molecular mediators of pain

A

PGE2 [feeever/pain] & Bradykinin

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123
Q

Cardinal signs of inflammation and pathophysiology

A
  1. Red: vasodilation [histamine, PG, bradykinin]
  2. Pain: bradykinin and PGE2 – sensitize
  3. Swelling: vascular permeability (histamine, tissue damage)
  4. Warmth: vasodilation
  5. Fever: IL-1, TNF (macrophages) –> COX/hypothalamus (PGEEE2)
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124
Q

Describe the molecular basis of fever

A

Pyrogens –> Macrophages (IL-1, TNF) –> COX/hypothalamus –> PGE2 increases temperature

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125
Q

The 3 phases of acute inflammation.

A
  1. Fluid/Edema
  2. PMN (24 hours)
  3. Macrophage (2-3 days)
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126
Q

What is the first step of neutrophil arrival? Second step? Step 3? Step 4?

A
  1. Margination [vasodilation slows blood flow in post capillary venules]
  2. Rolling: cells slow down with selectin speed bumps
  3. Adhesion
  4. Transmigration
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127
Q

P-selectin is upregulated by

A

Weibel-Palade bodies on endothelial cells W = VWF; P = P-selectin

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128
Q

E-selectin is induced by

A

E-selectin: TNF, IL-1

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129
Q

Selectins bind to __________ on leukocytes

A

Sialyl Lewis X

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130
Q

Cellular adhesion occurs with CAMS which bind to ________ on neutrophils

A

Integrins (C5a, LTB4 upregulate)

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131
Q

Leukocyte Adhesion Deficiency

  • Defect
  • Mode of inheritance
  • Classical clinical findings
A

AR recessive defect of integrins (CD18 subunit)

* Delayed separation of umbilical cord; increased PMN’s; recurrent bacterial infections that lack pus

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132
Q

What is pus?

A

Dead neutrophils sitting in fluid

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133
Q

Phagocytosis is enhanced by opsonins… (2)

A

IgG, C3b

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134
Q

Chediak-Higashi Syndrome defect and inheritance

A

AR protein trafficking defect; phagosome –> lysosome (RR system of MT are defective)

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135
Q

Chediak-Higashi Syndrome clinical features

A

Increased risk of pyogenic infections, neutropenia, giant granules in leukocytes, defective primary hemostasis, albinism, peripheral neuropathy

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136
Q

What are the 2 ways in which phagocytosed material is killed? Which is more effective?

A
  1. O2-dependent [more effective]; HOCl plays key role

2. O2-independent

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137
Q

Oxygen is converted to superoxide by:

A

NADPH oxidase

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138
Q

Superoxide is converted to H2O2 by:

A

Superoxide dismutase

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139
Q

H2O2 is converted to HOCL by:

A

MPO

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140
Q

CGD results in poor oxygen dependent killing 2/2

A

NADPH oxidase defect (XLR or AR)

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141
Q

CGD patients are most susceptible to infections by catalase positive organisms such as

A

S. aureus, Nocardia, Aspergillus, Pseudomas cepacia, S. marcessens; no longer have any source of H2O2 (could be salavaged from bacteria)

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142
Q

How do you screen for CGD?

A

Nitroblue tetrazolium test. Turns blue = NADPH oxidase in tact. Can you convert oxygen to superoxide?

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143
Q

Defective MPO results in an increased risk for what type of infection?

A

Candida [usually asymptomatic]; normal NBT test

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144
Q

O2 independent killing occurs via…

A

Enzymes present in 2ndary granules of leukocyte (lysozyme and MBP)

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145
Q

How do neutrophils die within tissue?

A

Apoptosis

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146
Q

How is acute inflammation resolved?

A
  • Resolution & healing (IL-10 and TGF-beta)
  • Continued acute inflammation (IL-8)
  • Abscess
  • Chronic inflammation
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147
Q

Which 2 cytokines shut down the acute inflammatory process?

A

IL-10 & TGF-beta

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148
Q

Chronic inflammation stimuli

A

Persistent infection, AI disease, foreign material, cancer

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149
Q

Activation of T cells requires 2 signals

A
  1. Binding of Ag/MHC

2. Second signal [B7 on APC binds to CD28 on CD4 T cell]

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150
Q

The second signal in activation of a CD4+ T cell

A
  1. EC Ag phagocytosed and presented via MHC2 (APC)

2. B7 (APC) on CD28 on CD4 T cell

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151
Q

Describe the B7/CD28 interaction

A

B7 on APC binds to CD28 on the CD4+ T cell

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152
Q

The 2 subsets of cytokines secreted by CD4+ T Cells

A
  1. TH1: CD8: IL2 (T cell growth factor), IFN-gamma (macrophages
  2. TH2: B-cells
    IL-4 (IgG/IgE class switching, 5, 10 (inhibits TH1)
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153
Q

Class switching cytokine

A

IL-4

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154
Q

Role of IL-5

A

Eosinophil chemotaxis and activation; maturation of B cells to plasma cells and class switching to IgA

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155
Q

IL-10

A

Inhibits Th1 cells

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156
Q

CD8+ T cells are activated by intra/extracellular Ag

A

Intracellular Ag

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157
Q

CD8 T cells kill targets with

A

Perforins, granzyme (induces apoptosis)

  • Activates caspase
  • Expression of FASL which binds FAS (activates apoptosis)
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158
Q

Naive B cells express surface (2 Ig’s)

A

IgM and IgD

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159
Q

How are B cells activated? 2 ways

A
  1. Ag–> surface IgM

2. B-cell to MHC 2 CD4/ CD40/CD40L

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160
Q

Granulomatous inflammation: the defining feature

A

Subtype of chronic inflammation: key cell = epitheloid histiocyte [macrophage with abundant pink cytoplasm]; surrounded by giant cells and rim of lymphocytes

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161
Q

Non-caseating granulomas lack _______________. Several examples of NC granulomas.

A

Central necrosis:

  1. Reaction to foreign material (implant)
  2. Sarcoid
  3. Beryllium exposure
  4. Crohn’s disease
  5. Cat Scratch disease
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162
Q

A stellate shaped non-caseating granuloma is caused by… (think ID)

A

Cat scratch disease

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163
Q

The DDx (2) for a caseating granuloma.

A

TB (AFB) or Fungal (Silver/GMS)

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164
Q

How are granulomas formed? 3 steps (name the major cytokines)

A
  1. Macrophage:CD4+ interaction
  2. IL-12/TH1 –> IFN-gamma [occurs in both caseating and non-caseating granulomas]
  3. Macrophage to epitheloid histiocyte
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165
Q

DiGeorge Syndrome is a developmental failure of ____________ due to ____________

A

3rd and 4th pharyngeal pouches 2/2 22q11 microdeletion

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166
Q

DiGeorge Syndrome p/w

A

T-cell deficiency (lack of thymus); hypocalcemia (PTH); abnormal heart, great vessels, face

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167
Q

SCID results from defective:

A

Cell mediated and humoral immunity

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168
Q

Etiologies of SCID include (3)

A
  1. Cytokine receptor defects
    * 2. ADA deficiency *
  2. MCH Class 2 deficiency
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169
Q

Treatment of SCID

A

Isolation & stem cell transplant

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170
Q

X-linked agammaglobulinemia

* Most common mutation

A

Complete lack of Ig 2/2 disordered B-cell maturation

* Bruton tyrosine kinase signalling molecule

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171
Q

X-linked agammaglobulinemia p/w

A

Bacterial, enterovirus (IgA/mucosal surfaces), and Giardia infections after 6 months of life; live vaccines must be avoided

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172
Q

Common variable immunodeficiency due to:
Patients p/w
Patients at increased risk for

A

B-cell or T-helper cell defect

  • Bacteria, enterovirus, Giardia
  • Present late childhood
  • AI + Lymphoma
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173
Q

IgA deficiency is the most common Ig deficiency; increased risk of…

A

Mucosal/viral infections

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174
Q

Which GI disease is associated with IgA deficiency?

A

Celiac disease

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175
Q

Hyper-IgM syndrome is due to…

A 
Mutated CD40L or CD40 Receptor; second signal cannot be delivered to helper T-cells during B-cell activation
* Cytokines necessary for Ig class switching are not produced; recurred pyogenic infections, especially at mucosal sites (IgA, IgG, IgE)
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176
Q

Wiskott-Aldrich Syndrome triad

A

TBOpenia, Eczema, Recurrent infections (humoral and cell-mediated)

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177
Q

Wiskott-Aldrich Syndrome inheritance and gene defect

A

X-linked WASP gene

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178
Q

C5-C9 deficiency increased risk for

A

Neisseria infection

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179
Q

C1 esterase inhibitor deficiency results in

A

Hereditary angioedema characterized by periorbital edema

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180
Q

The underlying principle of AI disorders

A

Loss of self-tolerance

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181
Q

Autoimmune polyendocrine syndrome triad

A 
* Central tolerance goes awry
AIRE mutation in the medullary epithelial cells in the thymus
1. Hypoparathyroidism
2. Adrenal failure
3. Candida
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182
Q

Positive selection; negative selection in the thymus. What part of the thymus does each occur?

A

Positive (Cortex): must recognize MHC and self-Ag

Negative (Medulla): bind self-Ag [dendritic cells and medullary epithelial cells]

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183
Q

Central tolerance in the bone marrow

A
  1. Receptor editing of light chain (RAG genes reexpressed)

2. Apoptosis

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184
Q

If central tolerance fails, the lymphocyte can still undergo negative selection in the periphery. How does this occur?

A

The second CD28/B7 signal does not occur. The CD4 T cell can undergo anergy or apoptosis.

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185
Q

CD95

A

FAS receptor (binds FAS Ligand) induces apoptosis

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186
Q

Autoimmune lymphoproliferative syndrome (ALPS)

A
  • Loss of peripheral tolerance

Mutations in the FAS apoptosis pathway. [FAS, FAS-L, caspase-10]

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187
Q

Tregs suppress immune responses in 2 ways.

A
  1. Block CD4+ cells (CTLA-4 on T-reg blocks B7)

2. Cytokines: IL-10 (limits MHC 2 and co-stimulator molecules), TGF-beta (inhibits macrophages)

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188
Q

The 3 types of Tregs.

A
  1. CD4+
  2. CD25+ (IL-2 Receptor)
  3. FOXP3 (Transcription factor)
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189
Q

CD25 polymorphisms are assoicated with which AI conditions?

A

MS, DM1 [Tregs]

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190
Q

FOXP3 mutations result in…

A

IPEX (Immune polyendocrineopathy, X-linked)

* Islets, DM1, diarrhea

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191
Q

Why do AI conditions occur in women of child bearing age?

A

Estrogen reduces apoptosis of self-reactive B-cells.

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192
Q

PTPN22 gene polymorphisms can result in…

A

Loss of self tolerance

Tyrosine phosphatase –> signalling mechanisms go awry and AI develops

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193
Q

SLE summary (Type 3 Hypersensitivity)

A

Decreased CH50, C3, C4

* Ab directed against host nuclear material and the complexes deposit in tissues, activating complement

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194
Q

Early complement deficiency (particularly C2) is associated with..

A

SLE b/c you need the early complement components to initiate the immune complex clearing process

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195
Q

Aside from a malar rash upon exposure to sunlight, SLE patients can present with this type of rash.

A

Discoid rash

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196
Q

The pancytopenia seen in SLE patients is a T2 or T3 hypersensitivity reaction?

A

T2

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197
Q

In Libman-Sacks endocarditis, vegetations on valves are on one or both sides of valves.

A

Both sides of valves

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198
Q

The 3 anti-phospholipid antibodies that are commonly tested clinically with SLE:

A
  1. Anticardiolipin (VDRL/RPR)
  2. Lupus anticoagulant (falsely elevated PTT b/c interferes with the test)
  3. Anti-beta-2-glycoprotein I
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199
Q

Antiphospholipid Ab syndrome [associated with SLE, but more commonly not associated with SLE]

A

Antiphospholipid Ab + hypercoagulable state; Arterial and venous thrombosis

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200
Q

The 3 classic drugs associated with anti-histone Ab+ SLE

A
  1. Hydralazine
  2. Procainamide
  3. INH
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201
Q

Most common causes of death in SLE (2).

A

Renal failure (MN or DPGN) and infection

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202
Q

T/F SLE patients have accelerated coronary atherosclerosis.

A

True

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203
Q

Sjogren’s syndrome: what type hypersensitivity reaction?

A

Type 4: AI destruction salivary and lacrimal glands (dry eyes, dry mouth, dental caries)

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204
Q

The most common AI condition associated with Sjogren’s syndrome

A

RA (can have RF in blood)

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205
Q

Anti-ribonucleoprotein Ab

A

Anti-SSA and Anti-SSB
Sjogren’s syndrome
* associated with extragrandular manifestations
* Risk of neonatal lupus and congenital heart block

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206
Q

Anti-SSA and neonates

A

Neonatal lupus and congenital heart block

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207
Q

Lymphocytic sialadenitis

A

Sjogren’s syndrome

Important to biopsy to R/O sarcoidosis, amyloidosis

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208
Q

Sjogren’s syndrome have an increased risk for…

A

B-cell lymphoma (presents as unilateral enlargement of parotid late in disease course)

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209
Q

Systemic sclerosis (Scleroderma)

A

AI damage of mesenchyme leads to fibroblast proliferation and collagen deposition
* Endothelin, PDGF, TGF-B

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210
Q

CREST syndrome

A 
Calcinosis (Anti-centromere Ab)
Raynaud
Esophageal dysmotility
Sclerodactyly
Telangiectasias of skin
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211
Q

DNA topoisomerase I Ab

A

Scleroderma

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212
Q

Most common cause of death in scleroderma

A

Lungs

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213
Q

Mixed connective tissue disease (name the Ab)

A

SLE, SS, polymyositis

ANA with serum Ab against U1 RNP

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214
Q

ANA with Anti-U1 RNP Ab

A

Mixed connective tissue disease

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215
Q

T/F Healing occurs via a combination of regeneration and repair.

A

True

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216
Q

Labile tissues continually regenerate. Give several examples and name where the stem cell layers are.

A

Bowl (crypts), skin (basal layer), bone marrow

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217
Q

CD34

A

Marker of hematopoietic stem cell

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218
Q

What is the marker of the hematopoetic stem cell?

A

CD34

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219
Q

What is the stem cell of the lung?

A

Type 2 pneumocyte

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220
Q

Stable tissues are quiescent, but can re-enter the cell cycle. Classic example is. Give a second example in the kidney.

A

Liver: compensatory hyperplasia 2/2 partial resection.

* Also PCT of kidney

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221
Q

Permanent tissues lack significant regenerative potential. The 3 examples:

A

Skeletal muscle, cardiac muscle, neurons

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222
Q

Repair replaces damaged tissue with a…

A

Fibrous scar

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223
Q

Why do scars appear on the skin?

A

Regenerative stem cells of the skin can be lost with a deep laceration

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224
Q

Granulation tissue consists of (3 components)

A
  1. Fibroblasts (collagen 3)
  2. Capillaries (nutrients)
  3. Myofibroblasts (contracts wound)
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225
Q

Eventually, collagen 3 is replaced with collagen type ___. What converts collagen 3? What is the co-factor?

A

1

Collagenase removes collagen 3 and requires Zn

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226
Q

Collagen 1

A

Bone

* Tensile strength

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227
Q

Collagen 2

A

Cartilage

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228
Q

Collagen 3

A

Pliable: BV (stretch), granulation tissue, embryonic tissue (stretch)

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229
Q

Collagen 4

A

Basement membrane

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230
Q 
These factors are important in repair/healing. State their purpose.
TGF-alpha
TGF-beta
PDGF
FGF
VEGF
A 
TGF-alpha: epithelial, fibroblast
TGF-beta: FGF, inhibit inflammation
PDGF: endothelium, smooth muscle, FGF
* FGF: angiogenesis *; skeletal development
VEGF: angiogenesis
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231
Q

Healthing by primary intention

A

Wound edges sutured together (minimal scar)

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232
Q

Healing by secondary intention

A

Edges are not approximated; granulation tissue fills in the defect (big scar & contraction of wound by myofibroblasts)

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233
Q

Delayed wound healing causes (think biochemistry)

A

Infection (most common cause)
Vitamin C [hydroxylation proline, lysine] , Cu [lysyl oxidase], Zn (collagen 3–>1)
* foreign body, ischemia, DM, malnutrition

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234
Q

GLY-Proline-Lysine gets hydroxylated in collagen by what cofactor? Why is this necessary?

A

Vitamin C; necessary for cross-linking

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235
Q

Dehiscence

A

Rupture of wound; most commonly seen in abdominal surgery

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236
Q

Hypertrophic scar vs. Keloid

A

Hypertrophic: collagen 1 in a wound
Keloid: Excess collagen 3 outside of wound & way out of proportion (ear-lobe classic location)

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237
Q

How can you determine clonality of cancer cells? What about B cells?

A

G6PD isoforms (G6PD on X chromosome); Androgen receptor isotypes; Ig light chain [kappa: lambda 3:1]

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238
Q

What is the normal ratio of kappa:lambda in a B cell?

A

3:1

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239
Q

The 3 DDX for LAD.

A
  1. Infection (reactive hyperplasia)
  2. Lymphoma
  3. Metastatic cancer
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240
Q

Are benign tumors monoclonal?

A

Yes

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241
Q 
Name the tumors (benign + malignant)
Epithelium
Mesenchyme
Lymphocyte
Melanocyte
A

Adenoma/Adenocarcinoma
Lipoma/Liposarcoma
( ) Lymphoma/Leukemia
Nevus/Melanoma

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242
Q

Causes of death in adults (3 major) & in children (3)

A
  1. Cardiovascular disease
  2. Cancer
  3. Cerebrovascular
    - –
  4. Accidents
  5. Cancer
  6. Congenital defects
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243
Q

Most common cancers in adults (incidence): 3

A
  1. Breast/prostate
  2. Lung
  3. Colorectal
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244
Q

Most common cancers in adults (mortality): 3

A
  1. Lung
  2. Breast/prostate
  3. Colorectal
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245
Q

Approximately how many cancer divisions occur before the earliest clinical symptoms arise?

A

30

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246
Q

T/F Each cancer division results in increased mutations. Cancers that do not produce symptoms until late will have undergone additional divisions and mutations. Cancers detected late have a poor prognosis

A

True

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247
Q

The 2 major goals of cancer screening.

A
  1. Catch dysplasia before it becomes carcnioma

2. Detect carcinoma before clinical symptoms arise

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248
Q

Tumor is driven by:

A

DNA mutations

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249
Q

Cancer: Aflatoxins

A

HCC

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250
Q

Cancer: Alkylating agents

A

L/L

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251
Q

Cancer: Alcohol

A

SCC OP, upper esophagus, pancreatic, HCC

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252
Q

Cancer: Aresnic

A

SCC skin, lung cancer, angiosarcoma liver

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253
Q

Cancer: Asbestos

A

Lung cancer; mesothelioma

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254
Q

Cancer: Cigarette smoke

A

OP cancer, esophagus, lung, kidney, bladder

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255
Q

Cancer: Nitrosamines

A

Stomach carcinoma

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256
Q

Cancer: Napthylamine

A

Urothelial carcinoma of bladder

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257
Q

Cancer: Vinyl chloride (PVC pipes)

A

Angiosarcoma of the liver

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258
Q

Cancer: Nickel, Chromium, Beryllium, Silica

A

Lung carcinoma

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259
Q

Cancer: EBV

A

NP carcinoma [Chinese, African], BL, CNS lymphoma (AIDS)

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260
Q

Cancer: HHV-8

A

KS [endothelial cells]

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261
Q

Cancer: HBV, HCV

A

HCC

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262
Q

Cancer: HTLV-1

A

Adult T-cell leukemia, lymphoma

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263
Q

Cancer: HPV 16, 18, 31, 33

A

SCC vulva, vagina, anus, cervix (AC cervix)

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264
Q

Cancer: ionizing radiation [nuclear reactor]

A

AML, CML, Papillary carcinoma of the thyroid [hydroxyl free radicals]

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265
Q

Cancer: nonionizing radiation (UVB)

A

Basal cell carcinoma, SCC, melanoma [pyrimidine dimers in DNA, normally excised by restriction endonuclease]

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266
Q

3 key regulatory systems disrupted in cancer

A
  1. Proto-oncogenes
  2. Tumor suppressor genes
  3. Regulators of apoptosis
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267
Q

Mutations of proto-oncogenes form…

A

Oncogene: unregulated cell growth

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268
Q

4 categories of oncogenes

A
  1. Growth factors (PDGF)
  2. Growth factor receptors (EGFR, RET, KIT)
  3. Signal transducers (RAS, ABL)
  4. Cell cycle (CDK) and nuclear regulators (MYC)
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269
Q

Cancer associated with PDGF-B mutation

A

Platelet dervied growth factor: Astrocytoma

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270
Q

Cancer associated with EGFR (Her2Neu) amplification

A

Breast cancer

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271
Q

Cancer associated with RET point mutation

A

MEN 2A, 2B [sporadic MTC]

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272
Q

Cancer associated with KIT point mutation

A

GIST

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273
Q

Cancer associated with RAS gene family

A

Carcinomas, melanoma, lymphoma (GTP binding protein – inability to cleave RAS GTP to make RAS GDP)

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274
Q

Cancer associated with ABL

A

t(9, 22) with BCR-ABL [CML and some forms of ALL]

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275
Q

Cancer associated with c-MYC TF

A

Burkitt’s Lymphoma t(14,18)

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276
Q

Cancer associated with N-MYC TF

A

Neuroblastoma

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277
Q

Cancer associated with L-MYC TF

A

SCLC

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278
Q

Cancer associated with cyclin D1

A

t(11,14) Mantle cell lymphoma

G1-S phase transition

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279
Q

RAS in OFF state = (GDP or GTP)

A

RAS-GDP

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280
Q

RAS in ON state = (GDP or GTP)

A

RAD-GTP

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281
Q

Cancer associated with CDK4

A

Melanoma

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282
Q

Histologic features of Burkitt’s lymphoma

A

Starry sky appearance

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283
Q

In a lymph node, the 3 areas of B cells include (think lymphoma)

A

Follicle, Mantle, Margin

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284
Q

The 2 major tumor supressor genes

A

p53, Rb

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285
Q

p53 regulates which transition in the cell cycle?

A

G1-S phase transition

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286
Q

BAX

A

Destroys BCL-2; allows cytochrome C to leak out of mitochondria and cause apoptosis (p53 allows)

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287
Q

Germline mutation in p53 results in what syndrome?

A

LiFraumeni syndrome: increased risk for multiple types of carcinomas and sarcomas

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288
Q

Rb regulates which transition in the cell cycle

A

G1-S phase

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289
Q

T/F Phosphorylated Rb is happy. It then releases E2F, which allows G1-S transition.

A

True

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290
Q

Who phosphorylates Rb?

A

Cyclin D

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291
Q

T/F A mutated Rb results in constitutively free E2F

A

True

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292
Q

Sporadic vs. Germline mutation of Rb; unilateral/bilateral

A

Sporadic: unilateral
Germline: B/L & osteosarcoma

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293
Q

BCL2 overespression occurs in what cancer?

A

Follicular lymphoma (t(14,18))

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294
Q

Telomerase is a necessary enzyme for cell immortality. Normally telomeres shorten and results in cellular senescence. Cancers have up/downregulated telomerase

A

Upregulated

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295
Q

T/F Angiogenesis is necessary for tumor growth survival

A

True

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296
Q

Why does immunodeficiency increase risk for cancer?

A

Downregulated MHC1 allows for evasion of immune surveillance

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297
Q

T/F Downregulation of e-cadherin can result in cancer spread. What are the next steps?

A

True

  1. Lamin (basement membrane)
  2. Collagenase 4
  3. Fibronectin
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298
Q

Which carcinomas spread via the blood?

A

RCC, HCC, choriocarcinoma, Follicular carcinoma thyroid

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299
Q

Omental caking is characteristic of

A

Ovarian carcinoma

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300
Q

T/F Immunohistochemistry is used to characterize different tumors.

A

True

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301
Q

Intermeidate filament immunohistochemical stain: Keratin

A

Epithelium

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302
Q

Intermediate filament immunohistochemical stain: Vimentin

A

Mesenchyme

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303
Q

Intermediate filament immunohistochemical stain: Desmin

A

Muscle

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304
Q

Intermediate filament immunohistochemical stain: GFAP

A

Neuroglia

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305
Q

Intermediate filament immunohistochemical stain: neurofilament

A

Neurons

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306
Q

Immunohistochemical stain: S-100

A

Melanoma

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307
Q

Immunohistochemical stain: Chromogranin [Differentiate between the best and worse differentiated types of this tumor]

A

Neuroendocrine cells
Best: Carcinoid
Worst: SCLC

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308
Q

Grading cancer takes into account the extent of

A

Differentiation

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309
Q

Staging cancer takes into account

A

Tumor size
Mets
Nodes

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310
Q

Paget’s disease of the breast indicates an underlying

A

Ductal carcinoma

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311
Q

Hemangioblastoma of retina, cerebellum, medulla with bilateral RCC

A

Von Hippel Lindau syndrome (Ch. 3)

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312
Q

Astrocytoma, Retinal Hamartoma, Hypopigmented spots and seizures

A

Tuberous sclerosis

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313
Q

Perivascular Homer-Wright Rosettes

A

Medulloblastoma

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314
Q

Pancoast tumor: SCC vs. Adenocarcinoma

A

SCC

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315
Q

Cafe au lait spots, Lisch nodule with a yellow-brown iris (Chromosome 17)

A

NF-1

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316
Q

B/L CN8 neuroma, juvenile cataracts (Chromosome 22)

A

NF-2

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317
Q

Port-wine stain with CN6 palsy

A

Sturge-Weber Syndrome

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318
Q

Colorectal & brain tumor

A

Turcot’s Syndrome

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319
Q

Colorectal polyposis and osteoma

A

Gardner’s syndrome

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320
Q

Microcephaly, micrognathia, polydactly, hypotonia

A

Patau Syndrome (Ch. 13)

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321
Q

Chromosome of Cri-du-Chat

A

5

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322
Q

Ank protein (ID)

A

Legionella

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323
Q

Thickened hyperpigmented skin with velvety texture

A

Basal cell carcinoma

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324
Q

Stable angina results in reversible/irreversible injury to myocytes?

A

Chest pain with exertion; reversible injury to myocytes

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325
Q

Stenosis at what % results in angina?

A

70%

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326
Q

Stable angina shows what on EKG?

A

ST depression

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327
Q

Which region of the heart muscle is most susceptible to ischemic damage?

A

Epi, Myo *** Endo

[Subendocardium]

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328
Q

The hallmark of subendocardial ischemia on EKG

A

ST-depression

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329
Q

Unstable angina results from…

A

Rupture of plaque: exposure of sub-endothelial collagen; partial occulusion

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330
Q

EKG findings unstable angina

A

ST-depression

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331
Q

Prinzmetal angina 2/2

A

Vasospasm of coronary artery

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332
Q

EKG findings Prinzmetal angina

A

ST-elevation [epicardium BV clamping down]

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333
Q

MI is 2/2

A

Necrosis of cardiac myocytes [rupture of plaque with TBX and complete occlusion]. Also due to vasospasm, emboli and vasculitis

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334
Q

The most common artery involved in an MI

A

LAD: anterior wall and anterior interventricular septum

335
Q

The most sensitive cardiac enzyme marker for an MI

A

Troponin I [up for 7-10 days]

336
Q

Why is CK-MB useful as a cardiac enzyme?

A

Detects reinfarction days after an MI; rises 6 hours after infarction, peaks at 24, normal by 3 days

337
Q

Treatment of MI

A

ASA/heparin, O2, nitrates, beta-blocker, ACEi

338
Q

Following an MI, fibrinolyis or angioplasty can cause… (2)

A
  1. Contraction band necrosis (Calcium returns to dead tissue)
  2. Reperfusion injury (free radicals); cardiac enzymes continue to rise
339
Q 
MI microscopic changes
< 4 hours
4-24 hours
1-3 days
4-7 days
1-3 weeks
1 month
A 
< 4 hours: none
4-24 hours: coag nex [dark discoloration]
1-3 days: PMN [yellow]
4-7 days: Macrophages [yellow]
1-3 weeks: Granulation

1 day: Coag nex
—pmns—
1 week: Macrophages
1 month: Scar

340
Q

Key complication < 4 hours following an MI

A

Cardiogenic shock, CHF, arrhythmia

341
Q

Key complication 4-24 hours following an MI

A

Arrhythmia

342
Q

Key complication 1-3 days following MI

A

Fibrinous pericarditis (transmural infarction)

343
Q

Key complication 4-7 days following MI

A

Rupture (cardiac tamponade, shunting, papillary muscle – MR)

344
Q

The papillary muscle of the heart is fed by what artery?

A

RCA

345
Q

3 major complications following a healed MI [6-8 weeks following an MI]

A
  1. Aneurysm
  2. Thrombus
  3. Dressler syndrome (anti-pericardium Ab)
346
Q 
Macroscopic changes following an MI
< 4 hours
4-24 hours
1-3 days
4-7 days
1-3 weeks
4+ weeks
A 
< 4 hours: none
4-24 hours: dark discoloration
Through 1 week: yellow
1-3 weeks: red band (granulation)
>4 weeks: white scar
347
Q

Can you see fibrinous pericarditis with a subendocardial infarction?

A

No; only with a transmural infarction

348
Q

90% of patients who present with sudden cardiac death have pre-existing

A 
Severe atherosclerosis (MVP, CM, cocaine)
* Due to sudden ventricular arrhythmia
349
Q

L-sided CHF etiology

A

Ischemia, HTN, dilated CM, MI, restrictive CM

350
Q

What are heart failure cells?

A

Hemosiderin-iron laden macrophages seen in the lung

351
Q

The mainstay treatment of CHF

A

ACEi

352
Q

What is the underlying pathophysiology of cor pulmonale?

A

Hypoxic vasoconstriction leads to an overworked RV

353
Q

Nutmeg liver

A

RHF

354
Q

Most common congenital heart defect. Associated with FAS

A

VSD

355
Q

Eisenmenger syndrome

A

Reversal of a L-R congenital shunt: RVH, polycythemia, clubbing

356
Q

Most common type of ASD. Which one is associated with Down’s Syndrome?

A

Ostium secundum

* Ostium primum

357
Q

A split S2 on auscultation

A

ASD (delayed closure of pulmonic valve)

358
Q

What is a paradoxical embolus?

A

DVT –> through an ASD into the systemic circulation

359
Q

PDA is associated with which maternal infection?

A

Rubella

360
Q

The ductus arteriosus connects…

A

Pulmonary artery and aorta

361
Q

Holosystolic machine-like murmur

A

PDA

362
Q

Eisenmenger syndrome of a PDA results in…

A

Lower extremity cyanosis

363
Q

Which drugs close PDA vs. keeps it open

A

Close: indomethacin (decreases PGE –> PDA closure)

364
Q

Tetralogy of Fallot results in what type of shunt?

A

PA stenosis, RVH, VSD, overriding aorta [R–>L]

* Relieved by squatting to increase arterial resistance

365
Q

The degree of the _________ determines the extent of shunting and cyanosis in a TOF patient.

A

Stenosis

366
Q

A boot shaped heart on CXR

A

TOF

367
Q

Transposition of the great vessels can be managed (temporarily) with what treatment (non-surgical)

A

Aorta/Pulmonary artery switched: only survival –> maintain PDA with PGE2

368
Q

Transposition of the great vessels is associated with what maternal condition?

A

Maternal diabetes

369
Q

Truncus arteriosus

A

Single large vessel arising from both ventricles; truncus fails to divide

370
Q

Tricuspid atresia is associated with what septal defect?

A

ASD

371
Q

Infantile vs. Adult coarctation of the aorta

A

Infantile: PDA [proximal to the PDA]; associated with Turner syndrome [cyanosis LE]

Adult: not associated with PDA [HTN UE, hypotension LE]; rib notching

372
Q

Infantile coarctation of the aorta is associated with what syndrome?

Adult form of coarctation of the aorta has what odd association?

A

Turner syndrome; bicuspid aortic valve

373
Q

Most common overall cause of bacterial endocarditis.

A

S. viridans [infects previously damaged valves]

374
Q

Describe the pathogenesis of subacute bacterial endocarditis

A

Exposure of subendothelial collagen; thrombotic vegetations (platelets and fibrin); transient bacteriemia leads to TRAPPING of bacteria in vegetations

375
Q

IVDU acute endocarditis infects which valve?

A

Tricuspid valve

376
Q

Key bug that causes endocarditis of prosthetic valves

A

S. epidermidis

377
Q

Key bug that causes endocarditis in patients with underlying colorectal carcinoma

A

S. bovis

378
Q

Culture negative endocarditis

A

HACEK

* Hemophilus, Actinobacillus, Cardiobacterium, Eikenella, Kingella

379
Q

Consequences of septic embolization of cardiac emboli.

A

Janeway lesions: painless

Osler nodes: painful IC deposition

380
Q

Nonbacterial thrombotic endocarditis can be associated with… (2 conditions)

A

Hypercoagulable state, underlying adenocarcinoma

381
Q

Most common form of cardiomyopathy.

A

Dilated (systolic/bi-ventricular)

382
Q

High yield causes of dilated cardiomyopathy.

A

Genetic mutations (AD), myocarditis (Coxsackie), ETOH abuse, drugs (cocaine, doxorubicin), pregnancy

383
Q

Treatment of dilated cardiomyopathy.

A

Transplant

384
Q

AD cause of hypertrophic cardiomyopathy

A

Sarcomere (beta-myosin heavy chain)

385
Q

Histologic hallmark of hypertrophic cardiomyopathy

A

Myofiber disarray

386
Q

Causes of restrictive cardiomyopathy.

A

Amyloidosis, Sarcoidosis, Hemochromatosis, Loeffler syndrome (Ascaris), Endocardial fibroelastosis (children)

387
Q

Loeffler syndrome

A

Ascaris; can p/w restrictive CM

388
Q

Restrictive cardiomyopathy EKG findings

A

Low voltage EKG with diminished QRS amplitudes

389
Q

Most common primary cardiac tumor in adults

A

Cardiac myxoma

* Benign mesenchymal proliferation with a gelatinous appearance; abundant ground substance on histology

390
Q

Where does cardiac myxoma grow and what would the patient p/w?

A

Pedunculated mass in left atrium; syncope

391
Q

Benign hamartoma of cardiac ventricular muscle (association with what syndrome – children).

A

Rhabdomyoma; associated with tuberous sclerosis

392
Q

Mets to the heart usually results in

A

Pericardial effusion (breast, lung cancer, melanoma, lymphoma)

393
Q

Acute rheumatic fever & molecular mimicry. Explain

A

M proteins resemble proteins in human tissues = molecular mimicry

394
Q

JONES Criteria

A 
J: Joint problems (mig poly)
O: pan carditis
N: nodules SC
E: erythema marginatum
S: chorea
395
Q

Aschoff body with Anitzkow cells

A

Rheumatic fever myocarditis: focus of chronic inflammation with Anitzkow cells (histiocytes with caterpillar nucleus)

396
Q

What is the one thing that will kill a patient with acute rheumatic fever?

A

Myocarditis; Aschoff body with Anitzkow cells

397
Q

Chronic rheumatic valvular stenosis involves which valve?

A

Mitral valve; scarring of the valve with fusion of the commisures

398
Q

Does bicuspid valve predispose you to AS?

A

Yes (think adult coarctation of the aorta)

399
Q

In order to prove rheumatic heart disease, one valve MUST be involved: mitral or aortic.

A

Mitral

400
Q

Can microangiopathic hemolytic anemia be caused by aortic stenosis?

A

Yes

401
Q

What is the most common cause of aortic regurgitation?

A

Dilation of the aorta [think aortic aneurysm]

402
Q

Early, blowing diastolic murmur

A

AR

403
Q

Hyperdynamic circulation

A

Regurgitation of blood, SV increases, SBP increases, DBP decreaes (PP widens); bounding pulses, head bobbing, pulsatile nail beds

404
Q

Eccentric hypertrophy vs. Concentric hypertrophy

A

Eccentric: volume overloaded
Concentric: pressure overload

405
Q

Mitral valve prolapse

A

Associated with Marfan’s, EDS

406
Q

Mid-systolic click

A

MVP

407
Q

Holosystolic blowing murmur

A

Mitral regurgitation

408
Q

Opening snap followed by diastolic rumble

A

Mitral stenosis

409
Q

Innermost layer of a blood vessel; Middle and outermost

A

Tunica intima (endothelial cells on a BM), media (smooth muscle), adventitia (C/T)

410
Q

Organ ischemia can occur through

A

Thrombosis, Fibrosis

411
Q

Giant cell arteritis

A

> 50 y.o. females; branches of carotid artery [flu like, polymyalgia rheumatica]

412
Q

Polymyalgia rheumatica

A

Giant cell arteritis

413
Q

Bx findings giant cell arteritis

A

Granulomatous vascultis with intimal fibrosis; segmental vasculitis (negative bx doesn’t always R/O disease)

414
Q

Takayasu arteritis

A

Same disease as GCA; adults < 50 years old (young Asian female)

  • Aortic arch at branch points
  • Pulseless disease
415
Q

Which large vessel vasculitis is considered pulseless disease in young Asian females?

A

Takayasu arteritis

416
Q

Medium vessels arteries involve (what type of artery)

A

Muscular arteries

417
Q

Polyarteritis nodosa spares what organ? Is associated with what Ag?

A

Necrotizing vasculitis; lungs spared; HTN (renal); abdominal pain (mesenteric artery); HbSAg

418
Q

A string-of-pearls appearance within a context of varying degrees of fibrinoid necrosis and fibrosis is characteristic of which vasculitis?

A

Polyarteritis nodosa (PAN)

419
Q

Highlighter pink of a blood vessel wall is characteristic of which type of vascular injury?

A

Fibrinoid necrosis

420
Q

Kawasaki disease

A

Asian children < 4 y.o.; fever, conjunctivitis, rash palms/soles, cervical LAD
* Thrombosis with MI/aneurysm with rupture

421
Q

Treatment of Kawasaki disease

A

ASA, IVIG

422
Q

Under what circumstance do you use ASA to treat a child with a ‘viral’-type illness?

A

Kawasaki disease

423
Q

Which vasculitis in children is associated with a palmar/sole rash?

A

Kawasaki

424
Q

Buerger disease

A

Necrotizing vasculitis involving digits; presents with ulceration, gangrene, autoamputation of fingers and toes

  • Raynaud phenomenon is often present
  • Highly associated with smoking
425
Q

Wegener’s granulomatosis

A

Nasopharynx, lungs, kidneys (RPGN); C-ANCA+; cyclophosphamide

426
Q

Large necrotizing granulomas with necrotizing vasculitis in NP, lungs, kidney; key treatment?

A

Cyclophosphamide (Wegener’s)

427
Q

Microscopic polyangiitis is similar to Wegener’s. What are the differences?

A

Necrotizing vasculits involving multiple organs, lung and kidney
* No NP involvement and no granulomas (P-ANCA)

428
Q

Churg-Strauss Syndrome is distinguised from microscopic polyangiitis with which 3 features? Both are p-ANCA positive.

A
  1. Granulomas
  2. Asthma
  3. Eosinophilia
429
Q

Palpable purpura on buttocks and legs; gi pain/bleeding; hematuria; follows URTi

A

HSP / IgA Nephropathy

430
Q

Renal artery stenosis (lab value of importance; finding on CT)

A
  • Increased renin

* Unilateral atrophy

431
Q

2 high yield causes of renal artery stenosis (elderly male vs. young female)

A
  1. Atherosclerosis

2. Fibromuscular dysplasia

432
Q

Acute renal failure, headache, papilledema

A

Malignant htn emergency

433
Q

3 pathologic patterns of arteriosclerosis

A
  1. Atherosclerosis [intima]
  2. Arteriolosclerosis
  3. Monckeberg medial sclerosis [media]
434
Q

Hyaline vs. Hyperplasitc arteriolosclerosis

A

Hyaline: protein
Hyperplastic: smooth muscle

435
Q

4 most common arteries affected by atherosclerosis

A

Abdominal aorta, Coronary, Popliteal, ICA

436
Q

4 modifiable risk factors for atherosclerosis

A
  1. HTN
  2. HLD
  3. Smoking
  4. DM
437
Q

Fatty streak in blood vessels

A

Seen in teenagers (early atherosclerosis)

438
Q

Symptomatic atherosclerosis occurs with critical stenosis at what percentage?

A

70%

439
Q

Hallmark of atherosclerotic embolus

A

Cholesterol cleft

440
Q

Hyaline and hyperplastic; arteriolosclerosis causes

A
  1. Hyaline: proteins [pink] - benign HTN/DM (NEG-leaky)

2. Hyperplastic: malignant HTN

441
Q

Glomerular scarring 2/2 benign HTN.

* Histologic hallmark of arteriole.

A

Hyaline arteriosclerosis of renal arteriole

442
Q

Onion-skin hyperplastic arteriolosclerosis is 2/2

A

Malignant HTN

443
Q

Flea-bitten appearance of kidney

A

Fibrinoid necrosis 2/2 malignant hypertension

444
Q

Monckeberg medial calcific sclerosis

A

Non-obstructive; non clincally significant; incidental finding on X-ray or Mammography

445
Q

Aortic dissection is 2/2

What is the histologic hallmark?

A

Intimal tear 2/2 HTN

* Occurs within the context of pre-existing weakness of the media

446
Q

Vaso vasorum are present in which tunica in the proximal 10cm of the aorta?

A

Adventitia

Hyaline arteriosclerosis of vasovasorum; decreased Q to the outer part of blood vessel wall

447
Q 
Sharp, tearing, chest pain that radiates to the back;
#1 cause of death
A 
Aortic dissection;
Cardiac tamponade (dissection backwards); rupture into mediastinum (hemorrhage); ruptre forwards (renal artery compression)
448
Q

What is the highest yield cause of a thoracic aneurysm? Complications?

A

Balloon-like dilation of the thoracic aorta

  • Tertiary syphillis; tree-bark appearance of aorta
  • Aortic insufficiency (#1), compression of mediastinal structures, thrombosis/embolism
449
Q

AAA occurs 2/2 atherosclerosis in what part of the aorta?

A

Below renal arteries, but above the bifurcation

450
Q

A pulsatile abdominal mass that grows with time. What is the critical size most associated with rupture? What are the S/S of rupture?

A

AAA

> 5 cm; Hypotension, pulsatile mass, flank pain

451
Q

T/F Hemangioma often regresses during childhood. Is it blanching?

A

True; Benign tumor of BV

Yes, blanches (vs. purpura which doesn’t blanch)

452
Q

Angiosarcoma is a malignant proliferation of endothelial cells. Liver angiosarcoma is associated with…

A

PVC, Arsenic, Thorotrast

453
Q

Low-grade malignant proliferation of endothelial cells. Is it blanching?

A

KS (HHV-8)

* Can involve skin/visceral organs [non-blanching]

454
Q

KS is seen in… (3 different patient demographics). How do you treat each group?

A

E. European males (surgery), AIDS (ARV), transplant recipients (decreased IS)

455
Q

Cystic tunica medial necrosis

A

Dissection

456
Q

Rheumatic fever is associated with Aschoff bodies which are…

A

Noncaseating granulomas with giant cells

457
Q

Most commmon cause of rhinitis

A

Adenovirus

458
Q

Allergic rhinitis is associated with…

A

Asthma and eczema

459
Q

Nasal polyps occur in… (3 conditions)

A

Cystic fibrosis, ASA-intolerant asthma, repeated bouts of rhinitis

460
Q

Profuse epistaxis in adolescent males

A

Angiofobroma (benign tumor of nasal mucosa composed of large blood vessels and fibrous tissue)

461
Q

Nasopharyngeal carcinoma with cervical LAD is associated with which virus in which 2 demographics?

A

EBV: African children and Chinese adults [pleomorphic keratin-positive epithelial cells in the background of lymphocytes]

462
Q

Acute epiglottitis caused by which microbe?

A

H. flu type B [high fever, sore throat, droling, dysphagia, acute airway obstruction]

463
Q

Croup [hoarse barking cough and inspiratory stridor] is caused by…

A

Parainfluenza virus

464
Q

Vocal cord nodules 2/2

A

Excessive use; myxoid degeneration [resolves with rest]

465
Q

Laryngeal papilloma is due to which virus? Single/Double; Adults/Children

A

HPV 6 & 11 [single in adults; multiple in children]

466
Q

Laryngeal carcinoma risk factors…

A

ETOH, tobacco

467
Q

Parietal and visceral pleura are lined by what type of cells?

A

Mesothelial cells

468
Q

Spontaneous PTX; tracheal shift

A

Rupture of emphysematous bleb in a young male [shift toward the side of PTX]

469
Q

Tension PTX; tracheal shift

A

Shift to opposite side of injury 2/2 penetrating chest injury

470
Q

Mesothelioma p/w

A

Recurrent pleural effusions, chest pain [massive encasement of the lung]
2/2 asbestos exposure

471
Q

Pulmonary HTN histopathology

A
  1. Atherosclerosis of pulmonary trunk
  2. Smooth muscle hypertrophy
    * * 3. Plexiform lesions tuft of capillaries**
472
Q

Young female p/w exertional dyspnea

A

Pulmonary hypertension

473
Q

Familial forms of pulmonary hypertension is associated with inactivating mutations of…

A

BMPR2 [leads to proliferation of vascular smooth muscle]

* Plexiform lesions

474
Q

Recurrent PE can lead to…

A

Pulmonary HTN

475
Q

ARDS histologic hallmark & CXR classical findings

A

Leaking of protein rich fluid: hyaline membranes

* White out

476
Q

Ventilator setting in ARDS

A

PEEP: positive end-expiratory pressure

477
Q

Recovery in ARDS can lead to interstitial fibrosis because…

A

You’ve knocked out the type 2 pneumocytes [stem cells]

478
Q

Neonatal RDS arises 2/2

  • X-ray finding
  • Associated with
A

Inadequate surfactant levels

  • Diffuse granularity of lung
    • Prematurity L:S ratio (low <2), C-section, maternal DM
479
Q

Major component of surfactant

A

Phosphatidylcholine = Lecithin

480
Q

T/F Steroids promote the development of surfactant.

A

True

481
Q

Insulin inhibits/promotes surfactant production

A

Inhibits

482
Q

Hypoxemia in a neonate increases the risk for..

Supplemental O2 increases risk for…

A

Persistence of PDA, necrotizing enterocolitis; supplemental O2 increases risk of free radical injury [blindness]

483
Q

Radon associated with which cancer…

A

Lung cancer

484
Q

In the Western US, you would think of what infectious cause of a coin lesion?

A

Histoplasma

485
Q

A benign mass of disorganized lung tissue + cartilage seen as a calcified mass on X-ray

A

Hamartoma

486
Q

SCLC: surgical or radiotherapy

A

Radiotherapy

487
Q

Lung cancer subtypes (NSCLC)

  1. Glands/Mucus:
  2. Keratin pearls/Intercellular bridges
A
  1. AC
  2. Squamous CC
  3. Large cell
488
Q

Small cell

A

ADH, ACTH, LES

489
Q

Tumors start with “s” are associated with …

A
  1. Smokers
  2. Cental
  3. Paraneoplastic
490
Q

Squamous cell carcinoma is associated with which paraneoplastic syndrome?

A

PTHrP

491
Q

Most common lung tumor in non-smokers and female smokers

A

Adenocarcinoma

492
Q

Bronchioalverolar carcnioma arises from which type of cells?

A

Clara cells; not related to smoking (PNA like consolidation)

493
Q

Chromogranin+ lung tumor

A

Carcinoid [polyp like tumor; nests of cells]

494
Q

2 types of neuroendocrine tumor in lung

A
  1. SCLC (non-well-differentiated)

2. Carcinoid (well-differentiated)

495
Q

Cannonball tumors on lung imaging is usually indicative of primary malignancy of … (2)

A

Breast, colon; Mets

496
Q

Adrenal gland mets primary site of malignancy

A

Lung

497
Q

Complications of lung cancer (based on the anatomy of the lung)

A

Pleural involvement, obstruction of SVC, involvement RLN, phrenic nerve; Horner’s

498
Q

Which type of lung cancer most commonly spreads to involve the pleura (not mesothelioma)

A

Adenocarcinoma

499
Q

Decreased TLC, very low FVC, FEV1, but increased FEV1:FVC is characteristic of…

A

Restrictive lung disease

500
Q

Obesity can result in restrictive or obstructive lung disease.

A

Restrictive

501
Q

Bleomycin, Amiodarone, Radiation therapy can cause…

A

(Idiopathic) pulmonary fibrosis

502
Q

TGF-beta from injured pneumocytes can drive…

A

Idiopathic pulmonary fibrosis

503
Q

Subpleural –> Diffuse honeycombing of lung is characteristic of which lung disorder?

A

Idiopathic pulmonary fibrosis

504
Q

Pneumoconioses mediated by which cell in the lung?

A

I/S fibrosis 2/2 small particles chronic exposure; mediated by macrophages

505
Q

Coal workers pneumoconoisis

A

Carbon dust seen in coal miners; black lung

506
Q

Caplan syndrome

A

Coal workers pneumoconoisis associated with RA

507
Q

Anthracosis

A

Build-up of carbon (not clinically significant)

508
Q

Silicosis increaes risk for which infectious disease?

A

Exposure to sand-blasting and silica miners; impairs phagolysosome to form –> fibrotic nodules in upper lobes of lung; TB

509
Q

Aerospace industry exposure: non-caseating granulomas in lung, hilum

A

Beryllium

510
Q

Shipyard, construction, plumbers

A
  1. Fibrosis lung/pleura

2. Cancer lung/pleura

511
Q

Long rod-shaped particles with brown beads in the lung (Ferrigunous body)

A

Asbestos

512
Q

Asteroid body

A

Sarcoidosis non-caseating granuloma

513
Q

AA female p/w dyspnea, cough, elevated ACE, hypercalcemia [1-alpha hydroxylase can activate vitamin D]

A

Sarcoidosis

514
Q

Hypersensitivity pneumonitis

A

Granulomatous reaction to inhaled antigen; p/w fever, cough, dyspnea; chronic exposure to lead to I/S fibrosis
** Eosinophils

515
Q

4 COPD disorders

A

Obstruction to getting air out of the lung

  • Emphysema
  • Chronic bronchitis
  • Bronchiectasis
  • Asthma
516
Q

What is the only increased value on spirometry in COPD?

A

TLC

517
Q

Chronic bronchitis Reid Index

A

> 50%

518
Q

2 types of submucosal glands in the lung; normal ratio in the lung? What index is this called?

A

Serous, mucinous glands

< 40% [Reid index]

519
Q

Blue bloaters

A

Chronic bronchitis

520
Q

Destruction of alveolar air sacs occurs in what COPD? What is the underlying pathophysiology?

A

Emphysema

[loss of elastic recoil and collapse of the small airways; balloon vs. shopping bag]

521
Q

What are the 2 values increased on spirometry in COPD?

A

TLC, FRC

522
Q

Chronic bronchitis Reid Index

A

> 50%

523
Q

2 types of submucosal glands in the lung; normal ratio in the lung? What index is this called?

A

Serous, mucinous glands

< 40% [Reid index]

524
Q

Blue bloaters

A

Chronic bronchitis

525
Q

Destruction of alveolar air sacs occurs in what COPD? What is the underlying pathophysiology?

A

Emphysema
[loss of elastic recoil and collapse of the small airways; balloon vs. shopping bag]
* Protease / anti-protease imbalance

526
Q

Panacinar vs. Centriacinar emphysema; upper/lower lobes

A

Panacinar: A1AT deficiency [lower lobes] – ER of hepatocytes
Centriacinar: Smoking [upper lobes – smoke goes up]

527
Q

Round, purple globules in hepatocytes; associated with emphysema; PAS+

A

A1AT deficiency

528
Q

A1AT: accumulation of protein in what organelle of the hepatocyte

A

Endoplasmic reticulum

529
Q

Curschmann spirals admixed with Charcot-Leyden seen in…

A

Asthma;

  • Mucus plugging
  • Eosinophilic MBP
530
Q

Nasal polyps are classically seen in allergic rhitinis. Where else can they be seen in adults? Children?

A

ASA-intolerant: adults

CF: Children

531
Q

FRC emphysema vs. fibrosis

A

Emphysema: increased
Fibrosis: decreased

532
Q

Asthma is defined as…

A

Reversible airway bronchocontrsiction

533
Q

T/F Allergens induce Th2 in asthma.

A

True: Il-4 (class switch), 5 (eosinophils), 10 (inhibts Th1)

534
Q

Nasal polyps are classically seen in allergic rhitinis. Where else can they be seen in adults? Children?

A

ASA-intolerant: adults

CF: Children

535
Q

Permanent dilation of bronchioles and bronchi (larger airways) 2/2 necrotizing inflammation with damage to airway walls

A

Bronchiectasis; blow out of a straw vs. blowing out of a pipe

536
Q

T/F bronchiectasis can lead to secondary amyloidosis

A

True

537
Q

Conjoined kidneys connected at lower pole; ascension stopped by what artery?

A

Horseshoe kidney (IMA)

538
Q

Complication of unilateral renal agenesis

A

Hypertrophy of existing kidney; hyperfiltration increases risk of renal failure later in life

539
Q

Oligohydramnios is associated with…

A

Bilateral renal agenesis; lung hypoplasia; flat face with low set ears (Potter Sequence)

540
Q

Potter sequence is associated with…

A

Bilateral renal agenesis; lung hypoplasia, flat face with low set ears and extremity defects

541
Q

Noninherited, congenital malformation of renal parencyhma characterized by renal cysts and abnormal tissue (cartilage)

A

Dysplastic kidney

  • Non-inherited
542
Q

What is on the differential for ARPKD?

A

Dysplastic kidney (non-inherited)

543
Q

T/F ARPKD can p/w Potter Sequence

A

True

544
Q

A baby p/w portal hypertension

A

ARPKD (hepatic fibrosis)

545
Q

ADPKD extra-renal manifestations (3 key ones)

A

Berry aneurysm, hepatic cyst, MVP [increased renin]

546
Q

AD defect: cysts in medullary collecting ducts w/ parenchymal fibrosis in shrunken kidneys

A

Medullary cystic kidney disease

547
Q

Hallmark of acute renal failure

A

Azotemia

548
Q

BUN:Cr ratio in pre-renal ARF

A

> 15; tubular function intact

549
Q

BUN:Cr ratio in post-renal ARF

A

2%; urine osmolality < 500 (decreased ability to [urine]

550
Q

Injury and necrosis of tubular epithelial cells: brown, granular casts in urine

A

ATN (BUN:Cr < 15)

551
Q

2 major etiologies of ATN

A

Ischemic: B/S; PCT & Thick ascending limb of medulla
Toxic: PCT

552
Q

Toxic etiologies of ATN

A

AG, lead, myoglobinuria, ethylene glycol, radiocontrast dye, urate

553
Q

Drug induced hypersensitivity reaction of intersititum and tubules that results in ARF

A

Acute I/S nephritis

554
Q

Chronic analgesic abuse, DM, SC disease, sever acute pyelo can cause

A

Acute papillary necrosis

555
Q

Alkaline urine with ammonia scent UTI

A

Proteus

556
Q

Pyuria with negative urine culture suggests

A

Urethritis 2/2 Chlamydia trachomatis or N. gonorrhoeae

557
Q

Pt p/w fever, flank pain, WBC casts and leukocytosis

A

Pyelonephritis

558
Q

Chronic pyelo in a child is usually 2/2

A

VUR

559
Q

Renal cortical scarring with blunted calyces

A

Chronic pyelo

560
Q

Scarring at upper and lower poles of kidney

A

Chronic VUR

561
Q

Thyroidization of the kidney

A

Chronic VUR/pyelonephritis

562
Q

Colicky pain with hematuria and unilateral flank tenderness

A

Kidney stone

563
Q

Ca oxalate, Ca phosphate kidney stone

A

Most common; hypercalcemia; idiopathic hypocalciura

564
Q

What type of kidney stone is seen in Crohn’s disease and why?

A

Ca oxalate stone; Increased absorption of oxalate (binds Ca)

565
Q

AMP stone that results in a staghorn calculus is generally caused by..

A

Infection with Proteus, Klebsiella; can develop UTI’s –> surgical removal

566
Q

Radiolucent kidney stone

A

Uric acid; treat with hydration and alkalinization of the urine

567
Q

Cysteine stones are seen in children with

A

Cystinuria [can also form staghorn calculus]

568
Q

Staghorn calculus in an adult vs. child

A

Adult: Proteus, Klebsiella
Child: Cystinuria

569
Q

Most common causes of ESRF

A

DM, HTN, glomerular disease

570
Q

Most common cause of chronic rejection in a lung transplant patient

A

Destruction of the small airways

571
Q

Nausea, anorexia, pericarditis, platelet dysfunction, encephalopathy, deposition of urea crystals in skin

A

Azotemia

572
Q

EPO produced by what cells in the kidney?

A

Peri-tubular interstitial cells

573
Q

2 reasons ESRF patients develop hypocalemia

A
  1. Vitamin D

2. HyperPO4 binds free Ca

574
Q

Osteitis fibrosis cystica

A

2/2 hyper PTH

575
Q

Osteomalacia vs. Osteoporosis

A

Cannot mineralize osteoid; buffered metabolic acidosis from bone Ca

576
Q

T/F Patients with ESRF can develop cysts in the context of shrunken kidneys while on dialysis.

A

T

577
Q

Renal hamartoma comprised of blood vessels, smooth muscle and adipose tissue is increased in frequency in patients with what disorder (also causes seizures)

A

Renal angiomyolipoma; Tuberous sclerosis

578
Q

Triad of hematuria, palpable mass and flank pain

A

RCC

579
Q

T/F RCC can p/w L varicocele

A

T (Spermatic vein drains into L renal vein)

580
Q

What color is gross mass of RCC? Most common subtype?

A

Yellow; clear cell

581
Q

Pathogenesis of RCC

A

Loss of VHL (3P) tumor supressor gene [increased IGF-1 and increased HIF VEGF and PDGF]

582
Q

VHL disease inheritance & 2 cancers

A

AD; RCC & hemangioblastoma of cerebellum

583
Q

RCC typically spreads to which nodes?

A

Retroperitoneal

584
Q

Malignant kidney tumor comprised of blastema, primitive glomeruli and tubules and stromal cells in a child [p/w hematuria and HTN]

A

Wilms Tumor [WT1 mutation]

585
Q

WAGR syndrome

A

Wilms, Aniridia, Genital abnormalities, mental and motor retardation

586
Q

Beckwith-Wiedemann Syndrome

A

Wilms Tumor, neonatal hypoglycemia, muscular hemihypertrophy, organomegaly (tongue)

587
Q

Most common type of Lower UT cancer; #1 risk factor

A

Urothelial carcinoma; polycyclic hydrocarbons, napthylamine, azo dyes, LTM cyclophosphamide, phenacetin

588
Q

2 distinct pathways of urothelial carcinoma

A
  1. Papillary [low to high grade]

2. Flat [Begins as high grade]

589
Q

Which subtype of urothelial carcinoma is associated with early p53 mutations?

A

Flat

590
Q

Urothelial tumors typically display a field defect. What is this?

A

So many mutations develop over time leads to multifocal nature and recurrence

591
Q

SCC of the bladder 2/2

A

Chronic cystitis, Schistosoma hematobium [Middle Eastern Male], long standing nephrolithiasis

592
Q

Adenocarcinoma of bladder at the dome of the bladder arises 2/2

A

** Arises from urachal remnant **, cystitis glandularis, extrosphy

593
Q

Urachus

A

Yolk sac to fetal bladder [lined by glanduar epithelium]; its remnant can lead to AC of the bladder

594
Q

Hypercoagulable state in nephrotic syndrome 2/2

A

Loss of AT3

595
Q

T/F Minimal change disease can be associated with Hodgkins Lymphoma

A

True

596
Q

Disease: Effacement of foot processes of podocytes on EM 2/2 cytokine proliferation. What type of protein is lost?

A

Minimal change disease [selective loss of albumin]

597
Q

Most common cause of neprotic syndrome in AA & Hispanics? Common diseases?

A

FSGS

HIV, heroin, SCD

598
Q

FSGS immune complex deposits? Yes or No

A

No: negative IF

599
Q

Kidney disease associated with HBV, solid tumors, SLE, drugs (ie. NSAIDS, penicillamine)

A

Membranous Nephropathy

600
Q

Subepithelial spike and dome appearance; granular IF

A

Membranous nephropathy

601
Q

Thick capillary membranes on H&E with tram-track appearance; granular IF [Type I & 2]

A

MPGN
Type I: subendothelial [HBV, HCV – more often assoc. w tram tracks]
Type II: within BM [Anti C3 nephritic factor Ab / stabalizing Ab]

602
Q

Anti-C3 nephritic factor Ab (which stabilizes the C3 convertase and overactivates complement)

A

Type 2 MPGN

603
Q

Preferential hyaline arteriosclerosis in DM nephropathy in which vessel: afferent or efferent? What treatment is indicated to slow progression of hyperfiltration induced damage?

A

Efferent; ACE inhibitor helps because you don’t want to squeeze down too much on efferent vessel.

604
Q

M protein virulence factor and renal disease

A

PSGN

605
Q

Subepithelial humps on EM

A

PSGN

606
Q

RPGN IF

A
  1. GBM [linear]
  2. Granular
  3. Vasculitis [negative IF]
607
Q

Crescent in RPGN is composed of…

A

Fibrin & macrophages

[Not collagen]

608
Q

Granular IF means…

A

Immune complex deposition

609
Q

Diffuse proliferative GN (with subendothelial deposits) is seen in what systemic AI disease?

A

SLE

610
Q

CS vs. Microscopic polyangiitis

A

IN CS:

  1. Eosinophils
  2. Granulomatous inflammation
  3. Asthma
611
Q

Isolated hematuria with sensory hearing loss and ocular disturbances

A

Alport syndrome; inherited defect in collagen 4 (X-linked); thinning and splitting of GBM

612
Q

Developmental malformation; pancreas forms a ring around the duodenum; risk of duodenal obstruction

A

Annular pancreas

613
Q

Premature activation of _____________ leads to activation of other enzymes in acute pancreatitis.

A

Trypsin

614
Q

What types of necrosis do you see in acute pancreatitis?

A

Liquefactive necrosis of pancreas; fat necrosis of peri-pancreatic fat

615
Q

2 most common causes of acute pancreatitis

A
  1. ETOH (contracts sphincter)

2. Gallstones (ampulla)

616
Q

Automobile accident in child wearing a seatbelt can cause…

A

Acute pancreatitis.

617
Q

Measles, mumps or rubella: Acute pancreatitis

A

Mumps

618
Q

Lipase or amylase: which is better marker for acute pancreatitis?

A

Lipase [amylase from salivary gland]

619
Q

Persisentece of elevated amylase in the face of resolved acute pancreatitis

A

Pancreatic pseudocyst, abscess

620
Q

Most common causes of chronic pancreatitis [adults vs. children]

A
  1. ETOH: adults

2. CF: children

621
Q

Pancreatic AC arises from…

A

Pancreatic ducts

622
Q

2 major risk factors for pancreatic AC

A
  1. Smoking

2. Chronic pancreatitis

623
Q

Pancreatic cancer at the head of the pancreas can p/w [vs. body/tail]

A

Painless jaundice, pale stools and a palpable gallbladder; 2ndary DM

624
Q

Serum tumor marker for pancreatic AC

A

CA 19-9

625
Q

Failure to form or early destruction of extrahepatic biliary tree p/w neonatal jaundice and cirrhosis

A

Biliary atresia

626
Q

Precipitation of cholesterol or bilirubin in bile results in…

A

Gallstones; supersaturated, decreased lecithin or bile acids [solublize the choleterol]; stasis

627
Q

What is the classical drug that can lead to gallstones?

A

Cholestyramine

628
Q

Are cholesterol stones radiolucent or radioopaque?

A

Radiolucent

629
Q

T/F Estrogen increases activity of HMG CoA reductase.

A

True

630
Q

Bilirubin stones are radiolucent or opaque?

A

Opaque

631
Q

6 key complications of gallstones

A
  1. Biliary colic [waxing/waning]
  2. Acute cholecystitis
  3. Chronic cholecysitis [Rokitishinky-Ashoff sinus]
  4. Gallbladder cancer
  5. Ascending cholangitis (GNR)
  6. Gallstone ileus
632
Q

Lab value increased in acute cholecysitis [besides WBC]

A

Increased ALP

633
Q

Rokitishinky-Ashoff sinus

A

Chronic cholecystitis; mucosa diving down into the smooth muscle

634
Q

Late complication of chronic cholecystitis seen on X-ray

A

Porcelain gallbladder [dystrophic calcification]

635
Q

A gallstone ileus can lead to …

A

Fistula formation b/t the gallbladder and duodenum

636
Q

Cholecystitis in an elderly woman raises suspicion for…

A

Adenocarcinoma of the gallbladder

637
Q

Is UC bilirubin water soluble?

A

No

638
Q

Pitch black liver; what other condition has the same pathophysiology, but no black liver?

A

Dubin-Johnson Syndrome

* Rotor syndrome

639
Q

Pruritis in obstructive jaundice is 2/2

A

Plasma bile acids

640
Q

Viral hepatitis caused by viruses other than hepatitis…

A

EBV, CMV

641
Q

Which hepatitis virus in a pregnant woman is most worrisome?

A

HEV

642
Q

First serologic marker to rise in acute HBV infection; its presence >6 months defines chronic state

A

HBsAG

643
Q

The presence of which Ab defines resolved or immunized HBV infection?

A

HBsAB IgG

644
Q

HDV co-infection vs. superinfection. Which is more severe?

A

Superinfection (different times) is more severe than co-infection (same time)

645
Q

Fibrosis in cirrhosis is mediated by which type of cell?

A

Stellate cell (TGF-beta)

646
Q

Can cirrhosis lead to hypersplenism?

A

Yes

647
Q

3 patterns of pathology seen in alcoholic liver disease

A
  1. Fatty liver
  2. ETOH hepatitis (acetaldehyde)
  3. Cirrhosis
648
Q

Damaged intermediate filaments within hepatocytes

A

Mallory bodies

649
Q

AST or ALT is located in the mitochondria?

A

AST

650
Q

Damage in hemochromatosis is caused by…

A

Free radicals (Fenton reaction)

651
Q

The key regulatory step in iron absorption

A

Enterocyte [C282Y mutation in HFE]

652
Q

Cirrhosis, secondary DM, bronze skin, cardiac arrhythmia and gonadal dysfunction

A

Hemochromatosis

653
Q

Brown pigment in hepatocytes; one stains blue with Prussian blue

A

Iron vs. Lipofuscin (not blue)

654
Q

ATP7B gene mutated in…

A

Wilson disease

655
Q

Treatment of Wilson disease

A

D-penicillamine

656
Q

AI granulomatous destruction of intrahepatic bile ducts. Which antibody?

A

PBC; anti-mitochondrial Ab

657
Q

Inflammation and fibrosis of intra and extra-hepatic bile ducts; leads to periductal fibrosis with onion-skin appearance, beaded on imaging

A

PSC

658
Q

p-ANCA & UC association with which hepatic disease?

A

PSC

659
Q

PSC patients have an increased risk for

A

Cholangiocarcinoma

660
Q

Pathophysiology of Reye’s syndrome

A

Mitochondrial damage of hepatocytes

661
Q

What type of benign tumor of hepatocytes is associated with OCP usage?

A

Hepatic adenoma

662
Q

T/F HCC can lead to Budd-Chiari syndrome

A

T

663
Q

Hepatomegaly with a nodular free edge of the liver raises suspicion for…

A

Mets to the liver

664
Q

Failure of facial prominennces to fuse

A

Clef lip and palate

665
Q

Painful, superficial ulceration of oral mucosa. Arises in relation to stress, but often recurs. Characterized by grayish base surrounded by erythema

A

Aphthous ulcer

666
Q

Syndrome of recurrent aphthous ulcers, genital ulcers and uveitis. Due to immune complex vasculitis involving small vessels

A

Behcet syndrome

667
Q

Virus that remains dormant in the ganglia of the trigeminal nerve.

A

Herpes-1

668
Q

Major risk factors for SCC mouth (floor of mouth)

A

Tobacco, ETOH

669
Q

Leukoplakia vs. Erythroplakia (Which is most associated with squamous dysplasia?

A

Must bx to r/o carcinoma.

Erythroplakia (angiogenesis)

670
Q

Oral hairy leukoplakia on the lateral aspect of the tongue is due to what virus? Any risk for cancer?

A

EBV in AIDS patients (no increased cancer risk)

671
Q

Orchitis, pancreatitis, aspetic meningitis associated with what virus?

A

Mumps

672
Q

Does an elevated amylase in a patient with mumps suggest pancreatitis?

A

Not necessarily (salivary amylase)

673
Q

Inflammation of salivary gland usually due to S. aureus infection is called

A

Sialadenitis

674
Q

Benign tumor of stromal (cartilage) and epithelial (glands) tissue of salivary gland which presents as a mobile, painles, circumscribed mass at the angle of the jaw

A

Pleomorphic adenoma

675
Q

Why is there a high rate of recurrence of a pleomorphic adenoma?

A

Irregular margins

676
Q

Benign cystic tumor with abundant lymphocytes and germinal centers; arises in parotid

A

Warthin tumor

677
Q

Malignant tumor composed of mucinous and squamous cells. Usually arises in parotid and involves the facial nerve

A

Mucoepidermoid carcinoma

678
Q

Congenital defect resulting in connection between esophagus and trachea is called:

A

TEF; polyhydramnios

  1. Vomiting
  2. Polyhydramnois
  3. Abdominal distension
679
Q

Thin protrusion of esophageal mucosa, most often in the upper esophagus results in obstruction. P/W dysphagia for poorly chewed food.

A

Esophageal web [increased risk SCC]

680
Q

Esophageal web, beefy-red tongue (2/2 atrophic glossitis), severe iron deficiency anemia

A

Plummer-Vinson syndrome

681
Q

Outpouching of pharyngeal mucosa through an acquired defect in the muscular wall; arises above UES at junction of esophagus and pharynx. P/W dysphagia, obstruction and halitosis

A

Zenker diverticulum

682
Q

A Zenker diverticulum is a true or false?

A

False

683
Q

Painful hematemesis in an alcoholic or bulemic patient

A

Mallory-Weiss Syndrome

684
Q

Boerhaave syndrome

A

Rupture of esophagus; air in mediastinum (SC emphysema)

685
Q

Dilated submucosal veins in the lower esophagus 2/2 portal hypertension. Painless hematemesis.

A

Esophageal varices

686
Q

Most of the esophageal venous blood drains into the _________________ which then drains into the SVC

A

Azygous vein

687
Q

The left gastric vein drains into the _______________________.

A

Portal vein

688
Q

Painless vs. painful hematemesis

A

Painless: esophageal varices
Painful: MW

689
Q

1 cause of death in cirrhosis

A

Esophageal varices

690
Q

Disordered esophageal motility with inability to relax LES; 2/2 damaged ganglion cells in myenteric plexus. Known infectious association?

A

Achalasia [Bird-beak sign]

* Chagas disease

691
Q

Bird beak sign on barium swallow

A

Achalasia

692
Q

Where is the myenteric plexus?

A

In the muscularis layer between the inner circular and outer longitudinal muscular layers

693
Q

Chagas disease an the esophagus

A

Achalasia

694
Q

High LES pressure on esophageal manometry

A

Achalasia

695
Q

Sliding hiatal hernia [hourglass appearance]

A

Stomach herniates upward into the esophagus

696
Q

T/F Hiatal hernia is a risk factor for GERD

A

True

697
Q

Para-esophageal hernia

A

Much less common; bowel sounds in lower lung fields.

698
Q

Bowel sounds in lower lung fields as well as lung hypoplasia is usually due to:

A

Paraesophageal hiatal hernia

699
Q

Adult onset asthma usually 2/2

A

GERD [heartburn, tooth erosion]

700
Q

How can strictures appear in the esophagus?

A

Mucosal ulceration in GERD healed by fibrosis

701
Q

Most common esophageal cancer worldwide

A

SCC esophagus [ETOH, tobacco, hot tea, achalasia, web, injury]

702
Q

Lymph node spread: upper, middle, lower 1/3 esophagus

A

Upper: cervical
Middle: mediastinal or tracheobronchial
Lower: Celiac or gastric

703
Q

Congenital malformation of the abdominal wall; leads to exposure of abdominal contents

A

Gastroschisis

704
Q

Persistent herniation of bowel into the umbilical cord 2/2 failure of herniated intestines to return to body cavity. Contents are covered by peritoneum and amnion of UC

A

Omphalocele (Seeled)

705
Q

Congenital hypertrophy of pylorus p/w projectile non-bilious vomiting 2 weeks. Visible peristalsis; olive-like mass in abdomen.

A

Pyloric stenosis

706
Q

Acid damage to gastric mucosa 2/2 imbalance between mucosal defenses and acidic environment

A

Acute gastritis

707
Q

Curling vs. Cushing ulcer

A

Curling: burn
Cushing: increased ICP

708
Q

Why do critically ill patients get gastric ulcers?

A
  1. Hypovolemia leads to decreased clearance of acid and decreased mucosal protection
  2. Increased ICP: Inc. ACh
709
Q

3 receptors on parietal cells that can increase acid production

A
  1. Gastrin
  2. Histamine
  3. ACh
710
Q

Erosion vs. ulcer

A

Erosion: loss of epithelium
Ulcer: loss of mucosal layer

711
Q

AI destruction of parietal cells of body/fundus. Type 4 hypersensitivity. Antibodies are a side-effect of the damage

A

Chronic gastritis

  • Atrophy of mucosa
  • Achlorhydria [increased gastrin and G cell hyperplasia]
712
Q

What are the 4 key regions of the stomach?

A

Cardia, fundus, body, antrum

713
Q

Chronic inflammation of the stomach increases risk for…

A

Intestinal metaplasia (Peyer’s pataches) and gastric AC

714
Q

Describe the underlying reason for intestinal metaplasia in the stomach with chronic gastritis.

A

Peyer’s patches/inflammation

715
Q

Does H. pylori invade? What is the most common location in the stomach?

A

No; antrum

716
Q

What type of lymphoma is associated with H. pylori?

A

Marginal zone (MALT)

717
Q

Epigastric pain that improves with meals

A

Duodenal ulcer

718
Q

Brunner glands

A

Produce mucus; hypertrophied in duodenal ulcer

719
Q

Posterior duodenal ulcer rutpure can lead to (2):

A

Acute pancreatitis; gastroduodenal artery bleeding

720
Q

Which artery bleeds in a ruptured gastric ulcer?

A

Left gastric artery (lesser curvature)

721
Q

2 subtypes of gastric AC & risk factors

A

Intestinal: large, irregular ulcer (lesser curvature of antrum) – metaplasia, nitrosamines smoked foods, blood type A
Diffuse: signet ring/linitis plastica (desmoplasia: reactive stromal response); not associated with H.pylori, nitrosamines, blood type A

722
Q

Intestinal gastric AC is associated with blood type

A

A

723
Q

Acanthosis nigricans [axillary] or Leser-Trelat sign [dozens of subheroic keratoses] can be associated with which type of cancer?

A

Gastric AC

724
Q

Left supravlavicular LAD

A

Gastric AC

725
Q

Krukenburg tumor seen with which subtype of gastric AC?

A

Diffuse gastric AC

726
Q

Sister Mary Josheph nodule seen with which subtype of gastric AC?

A

Intestinal gastric AC

727
Q

Congenital failure of small bowel to canalize is associated with what syndrome?

A

Duodenal atresia; Down Syndrome

728
Q

Double-bubble sign on AXR

A

Duodenal atresia (bilious vomiting); polyhydramnios

729
Q

Meckel diverticulum is a true/false?

A

True; arises due to failure of vitelline duct to involute [nutrients]

730
Q

Passing meconium thorough the umbilicus

A

Failure of vitelline duct to involute 100%

731
Q

Rule of 2’s

A

2% population, 2 inches long, 2 feet from IC valve; 2 y.o., bleeding/volvulus/intussuception/obstruction

732
Q

Twisting of bowel along mesentary; classical locations in adult vs child

A

Volvulus (obstruction and infarction)

  • Adult: sigmoid colon
  • Child: cecum
733
Q

Telescoping of proximal segment of bowel into distal. P/W currant jelly stools. Common causes in children and adults

A

Intussception; children = lymphoid hpyerplasia [ileum with many Peyer’s patches]; adults = cancer

734
Q

T/F Small bowel is susceptible to ischemic injury

A

True; p/w abdominal pain, bloody diarrhea, decreased bowel sounds

735
Q

Marked hypotension can result in transmural or mucosal infacrction of small intestine?

A

Mucosal

736
Q

HLA DQ2, DQ8 is associated with which small bowel disease?

A

Celiac disease

737
Q

The role of tissue transglutaminase in celiac disease?

A

Deaminates glaidin

738
Q

Dermatitis herpetiformis

A

IgA deposition at tips of dermal papillae; Celiac disease

739
Q

Anti IgA Ab: endomysium, TTG, gliadin [can tests IgG in IgA deficiency patients]

A

Celiac disease

740
Q

Flattening of villi, hyperplasia of crypts with epithelial lymphocytes

A

Celiac disease

741
Q

Damage in celiac disease is typically in what part of the intestine?

A

Duodenum

742
Q

Small bowel carcinoma and T cell carcinoma can present in patients with…

A

Celiac disease (refractory despite good dietary control)

743
Q

Enteropathy associated T cell lymphoma

A

Celiac disease

744
Q

Damage in tropical sprue is most prominent in what part of intestine?

A

J, I. (Duodenum in celiac disease)

745
Q

Folate abosrbed

A

Jejunum

746
Q

B12 absorbed

A

Ileum

747
Q

PAS+ organisms in macrophage lysosomes of the gut

A

Whipple disease [LP of small bowel]

748
Q

Whipple disease p/w

A

Arthritis, valves, LN, CNS; Fat malabsorption & steatorrhea (lots of macrophages in LP, can’t bring in the chylomicrons)

749
Q

Abetalipoproteinemia

A

B-48: chylomicron

B-100: VLDL, LDL

750
Q

Chromgranin+ means

A

Neuroendocrine tumor

751
Q

Neuroendocrine tumor of the gut occurs in what part of the gut

A

Carcinoid tumor; small bowel

752
Q

Once a carcinoid tumor mets to the liver, it creates a patient who p/w

A

Bronchospasm, flusing, diarrhea [carcinoid syndrome]

753
Q

What are 2 triggering factors of carcinoid syndrome?

A

ETOH, Emotional stress

754
Q

Appendicitis in child vs. adult is 2/2

A

Child: lymphoid hyperplasia
Adult: fecalith

755
Q

Lead pipe sign vs. string sign on imaging

A

Lead pipe: UC

String sign: Crohn’s

756
Q

Smoking UC vs. Crohn’s

A

UC: protective

Crohn’s: increases risks

757
Q

Crypt abscess on histology with pseudopolyps and loss of haustra

A

UC

758
Q

P-ANCA is positive in what bowel disease?

A

?UC

759
Q

Bloody diarrhea: UC or Crohn’s

A

UC

760
Q

Granulomas: UC or Crohn’s

A

Crohn’s

761
Q

Cobblestoning: UC or Crohn’s

A

Crohn’s

762
Q

Stricturing and creeping fat: UC or Crohn’s

A

Crohn’s

763
Q

Malabsorption: UC or Crohn’s

A

Crohn’s

764
Q

Lead pipe sign in UC 2/2

A

Loss of haustra

765
Q

Hirschsprung disease is associated with what syndrome?

A

Down Syndrome

766
Q

Down Syndrome: small and large bowel

A

Small: duodenal atresia
Large: Hirschsprung disease

767
Q

Congenital failure of ganglion cells to descend [neural crest]

A

Hirschsprung disese

768
Q

Meissner’s vs.

Aurebach’s mysenteric plexus

A

Meissners: SM [blood flow, secretions]

Auerbach’s: peristalsis and relaxation

769
Q

Rectal suction biopsy reveals a lack of ganglion cells in Hisrschprung disease because…

A

Must look at submucosa

770
Q

Colonic diverticulum involves which layers?

A

Mucosa, Submucosa

771
Q

Colonic diverticulum arises 2/2 in what location?

A

Wall stress, constipation, low fiber; where vasa recta traverse the muscularis propria – weakened wall [sigmoid colon]

772
Q

Air or stool in the urine

A

Recto-vesico fistula 2/2 diverticulitis

773
Q

Hematochezia in an older adult in Right colon 2/2 acquired malformation of mucosal and submucosal capillary beds

A

Angiodysplasia

774
Q

AD disorder resulting in thin-walled blood vessels in nasopharynx and GIT

A

Hereditary teleangiectasia

775
Q

Ischemic damage to the colon, usually at the splenic flexure 2/2

A

Atherosclerosis of SMA; post-prandial pain and weight loss

776
Q

T/F Hyperplastic polyp of L colon is benign with no malignant potential. Has a serrated appearance on BX.

A

True

777
Q

T/F Adenomtous polyp is premalignant

A

True

778
Q

Describe the sequence of colon cancer development.

A

APC—>K-ras–>p53/inc. COX

779
Q

APC is on chromosome

A

5

780
Q

What over-the-counter drug can actually protect against colon cancer?

A

Aspirin (COX expression at the terminal end of adenoma-carcinoma sequence along with p53 mutation)

781
Q

> 2cm, sessile, villous adenomatous colon polpy: increased or decreased theoretical cancer risk

A

Increased [villous = villian]

782
Q

AD or AR: FAP

A

AD: Ch. 5

783
Q

FAP with fibromatosis and osteoma

A

Gardner’s syndrome (retroperit + bone)

784
Q

FAP with CNS tumors (medulloblastoma and glial tumor)

A

Turcot syndrome

785
Q

Sporadic hamartomatous benign poly that arises in children <5 y.o.; usually presents as soliarty rectal polyp that prolapses and bleeds

A

Juvenile polyp [large numbers in stomach and colon raise cancer risk]

786
Q

Hamartomatous polyps throughout the GIT with mucocutaneous hyperpigmentation on lips, oral mucosa and genital skin (AD)

A

Peutz-Jeghers Syndrome: increased risk for breast, colorectal and GYN cancer

787
Q

2 pathways of colon cancer

A
  1. Adenoma-carcinoma

2. MSI (MMR)

788
Q

Inherited mutation in DNA MMR repair enzymes; increased risk for colorectal, ovarian and endometrial carcinoma (Colorectal arises de novo R-sided)

A

HNPCC

789
Q

Decreased stool caliber, LLQ pain, blood-streaked: L or R colon ca

A

L

790
Q

Fe-deficiency anemia, vague pain: L or R colon ca

A

R

791
Q

Serum tumor marker for colon ca

A

CEA

792
Q

Breast is embryologically derived from

A

Skin

793
Q

Breast tissue can develop anywhere along

A

Milk line

794
Q

All ducts and lobules are lined by:

A

Luminal cell layer and myoepithelial cell

795
Q

T/F Breast tissue is hormone sensitive

A

T

796
Q

Anatomically, the highest density of breast tissue

A

UOQ

797
Q

Acute mastitis 2/2 breast feeding usually caused by..

A

S. aureus

798
Q

Subareolar mass with nipple retraction; Highly dependent on vitamin A; squamous metaplasia in the breast seen in a smoker.

A

Periductal mastitis

799
Q

Green-brown nipple discharge; inflammation of subareolar duct presents in multiparous post menopausal woman [plasma cells]

A

Mammary duct ectasia

800
Q

Fat necrosis [calcifications and giant cells] of breast that shows up as calcification on mammography 2/2

A

Trauma

801
Q

Cystic dilation of mammary ducts and/or terminal duct in a pre-menapausal woman (lumpy bumpy blue dome cyst)

A

Fibrocystic change

802
Q

Fibrocystic change: fibrosis, cysts and apocrine metaplasia. Any risk of ca?

A

No!

803
Q

Fibrocystic change: ductal hyperplasia & sclerosing adenosis. Any risk of ca?

A

Yes: 2x invasive carcinoma in either breast

804
Q

Fibrocystic change: atypical hyperplasia. Any risk of ca?

A

Yes: 5x invasive carcinoma in either breast

805
Q

Can sclerosing adenosis be calcified on mammography?

A

Yes

806
Q

Benign breast growth that bleeds in a pre-menapausal woman. What cells do you see?

A

Intraductal papilloma; fibrovascular core see both epithelial cells and myoepithelial cells

807
Q

How do you differentiate a benign intraductal papilloma from papillary carcinoma?

A

Ca: only one cell type [no myoepithelial cells] also in an older woman

808
Q

Tumor of fibrous tissue and glands; well circumscribed “mouse in the breast” that is estrogen sensitive in a pre-menopausal woman

A

Fibroadenoma

809
Q

Fibroadenoma-like tumor with overgrowth of fibrous component; leaf-like projections in post menopausal women

A

Phyllodes tumor

810
Q

Major risk factor for breast cancer

A

Estrogen exposure

* Female, age, early menarche/late menopause, obesity, atypical hyperplasia

811
Q

DCIS that reaches the nipple

A

Paget’s disease of the breast

812
Q

Major types of breast cancer

A

DCIS, LCIS

813
Q

What type of DCIS has high-grade cells with necrosis and dystrophic calcification in center of ducts?

A

Comedo type of DCIS

814
Q

How is DCIS seen on mammography?

A

Calcification

815
Q

3 potential pathologies of calcification on mammography?

A
  1. Fat nex
  2. Sclerosing adenosis
  3. DCIS
816
Q

Most common type of invasive carcinoma of breast that p/w breast mass detected by PE or mammography

A

Invasive ductal carcinoma

817
Q

Duct-like structures in desmoplastic stroma of breast bx

A

Invasive ductal carcinoma

818
Q

Subtypes of invasive ductal carcinoma

A

Tubular carcinoma
Mucinous carcinoma
Medullary carcinoma
Inflammatory carcinoma

819
Q

Subtype of invasive ductal carcinoma with a good prognosis

A

Tubular carcinoma

820
Q

Subtype of invasive ductal carcinoma with a good prognosis seen in elderly women

A

Mucinous carcinoma

821
Q

Subtype of invasive ductal carcinoma that p/w an inflammed breast that does not resolve with ABX; bx cancer w/in dermal lymphatics

A

Inflammatory carcinoma

  • Clincopathologic
  • DDX acute mastitis
822
Q

Subtype of invasive ductal carcinoma seen in pts with BRCA1 mutations

A

Medullary carcinoma

823
Q

Underlying pathology in LCIS

A

Dyscohesive cells lacking e-cadherin

824
Q

BRCA & E-cadherin

A

LCIS

825
Q

Multifocal and B/L: DCIS or LCIS

A

LCIS

826
Q

What type of breast cancer is often discovered incidentally?

A

LCIS [Tamoxifen and close follow-up]

827
Q

Breast cancer that grows in single-file pattern?

A

E-cadherin / invasive lobular carcinoma

828
Q

Most patients with BRCA don’t p/w mets. Therefore, the most useful factor in prognosis is…

A

Spread to axillary LN

829
Q

T/F Her2Neu is a cell surface receptor proto-oncogene.

A

T

830
Q

Triple negative cancer: positive or negative PGX. What demographic of women?

A

Negative: AA women

831
Q

BRCA1 or BRCA2: Breast cancer in males. What other syndrome?

A

BRCA2; Klinefelter syndrome

832
Q

BRCA1 mutations associated with which 2 cancers?

A

Breast, ovarian serous

833
Q

Highest density of breast tissue in a male

A

Sub-areolar

834
Q

Males develop ductal or lobular carcinoma

A

Ductal (males don’t develop lobules)

Step 1 Prep (15 decks)

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