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Step 1 > Pathoma Ch 6, 10, 14, 18 (WBC, GI, Male GU, MSK) > Flashcards

Pathoma Ch 6, 10, 14, 18 (WBC, GI, Male GU, MSK) Flashcards

6. WBC D/o 10. GI path 14. Male GU 18. MSK

1
Q

ALL vs. AML

(a) Cell marker
(b) Age on onset

A

ALL vs. AML- both acute leukemias (so blasts over 20% of bone marrow), but of the two different hematopoietic lineages

ALL = acute lymphoblastic leukemia

(a) tdt positive = DNA polymerase found only in lymphoblasts (not in myeloid blasts or mature lymphocytes)
(b) Children

AML = acute myeloid leukemia

(a) MPO (enzyme used in O2 dependent killing to catalyze H2O2 –> HOCl, so makes sense it would be seen in neutrophils and macrophage lineage)
- cystal aggregates of MPO = Auer rods
(b) Adults, like over 65

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2
Q

Gastroschisis vs. omphalocele

A

Gastrochisis = failure for anterior abdominal wall to properly fuse fully => abdominal contents herniate out, not surrounded by peritoneum

Omphalocele = persistent herniation of bowel into umbilical cord => failure of bowel to return during 90 degree rotation
-associated w/ cardiac complications

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3
Q

How to differentiate follicular lymphoma from follicular hyplerplasia (as a result of RA or early HIV)

(a) Tingible body macrophages
(b) Architecture of LN

A

Follicular lymphoma (neoplastic prolif) vs. follicular hyperplasia (hyperplastic prolif)

(a) Tingible body macrophages are eating up dead cells- won’t be seen in Follicular lymphoma b/c apoptosis is inhibited
(b) LN architecture in maintained in follicular hyplerplasia (follicles all on the periphery, just more of them and they’re bigger), while in follicular lymphoma the follicles take over the entire lymph node (into the cortex) and normal architecture of LN is not maintained

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4
Q

(a) Triad of Behcet syndrome

(b) Mechanism of disease

A

(b) Behcet syndrome = autoimmune vasculitis (immune complex inflammation of small vessels)

(a) Oculo-oro-genital syndrome
- recurrent apthous ulcers (canker sores), genital ulcers, and uveitis

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5
Q

CLL vs. Hairy Cell Leukemia

(a) Cell of origin
(b) Classic molecular marker or stain

A

Both are neoplastic proliferation of B cells

CLL

(a) Neoplastic proliferation of naive B cells
(b) CD5 and CD10 posiitve

Hairy Cell Leukemia

(a) Neoplastic proliferation of mature B cells
(b) TRAP stain positive

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6
Q

Differentiate acute and chronic leukemia

A

Acute leukemia = neoplastic proliferation of immature cells of the myeloid or lymphoid lineage

Chronic leukemia = neoplastic proliferation of mature circulating lymphocytes

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7
Q

MC form of Non Hodgkin Lymphoma

(a) Growth pattern
(b) Differentiation

A

DLBCL = diffuse large B cell lymphoma

(a) Grows diffusely in sheets
(b) Aggressive cancer b/c it’s poorly differentiated, larger the cell the less they are like the normal cell (so more poorly differentiated they are)

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8
Q

Name 3 complications of myeloproliferative disorders

A

Myeloproliferative disorders = neoplastic accumulation of mature cells of the myeloid lineage

3 complications

  1. transformation to AML
  2. bone marrow fibrosis
  3. increased risk of hyperuricemia and gout
    - 2/2 increased DNA turnover
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9
Q

Differentiate leukoplakia and hairy leukoplakia

A

Leukoplakia = white plaque that can’t be scared off (so not candida), pre-malignant lesion to squamous cell carcinoma of the mouth

Hairy leukoplakia = rough white patch on LATERAL tongue (lateral is key) in immunocompromised pts, 2/2 EBV infection
-EBV-induced squamous cell hyperplasia, NOT pre-malignant

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10
Q

2 tests to confirm H. pylori eradication

A
  1. Negative urea breath test
    - b/c H. pylori produced urease (and proteases), so urea will be present in breath
  2. lack of stool antigen
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11
Q

CML

(a) Protein responsible
(b) Tx
(c) Transformation to which acute leukemia?
(d) Key CBC finding

A

CML = chronic myeloid leukemia

(a) t(9,22) makes BCl-ABL fusion protein that is a constitutively active tyrosine kinase
(b) Tx = Imatinib to block tyrosine kinase activity
(c) If CML transforms to acute leukemia: 2/3 AML and 1/3 ALL
- key here that it’s not only AML!!!! b/c the mutation is in the hematopoietic stem cell, not the myeloid stem cell
(d) Leukocytosis specifically w/ basophilia

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12
Q

MC location for carcinoid tumor

A

Small bowel

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13
Q

MC subtype of Hodgkin Lymphoma

A

Nodular sclersois Hodgkin lymphoma (NSHL): LN divided by broad bands of fibrosis w/ Reed Sternberg cells in open spaces = Lacunar cells

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14
Q

Presentation of mumps infection

(a) Feared complication in teenagers

A

Mumps p/w b/l inflammed parotid glands

(a) Teenagers w/ mumps can develop orchitis that carries risk of sterility

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15
Q

Which myeloproliferative d/o has the lowest risk of hyperuricemia/gout?

A

Essential thrombocytopenia has the lowest risk of hyperuricemia/gout b/c the high turnover is of plts (no nuclear material), not of RBCs or granulocytes as seen in P. Vera and CML

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16
Q

When do carcinoid tumors cause carcinoid syndrome?

A

Only can cause carcinoid syndrome (bronchospasm, diarrhea, flushing from excess 5-HT) when the tumor’s drainage bypass the portal vein

So once the tumor mets to the liver and is drained by the hepatic vein, then 5-HT won’t be degraded into 5-HIAA by MAO in the liver (then 5-HIAA excreted in urine)

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17
Q

Pt w/ long standing celiac disease and very tight/adherent diet control presents w/ recurrent disease

Concern?

A

Late complications of celiac disease:

  • small bowel carcinoma
  • T-cell lymphoma

Key here is that Celiac disease is T-cell mediated, so causes rare lymphoma that is T-cell (almost all lymphomas are B cell!!)

These two late complications present as refractory disease despite good dietary control

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18
Q

Chronic autoimmune gastritis vs. H. pylori gastritis

(a) Risk of which malignancies?
(b) Location

A

(a) Both cause incrase risk of gastric adenocarcinoma (intestinal type) b/c chronic inflammation causes metaplasia to intestinal cells
- then H. pylori also increases risk of MALT lymphoma

(b) AI gastritis damages parietal cells which are concentrated in the body and fundus of the stomach. While H. pylori manifests MC w/ inflammation of the antrum

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19
Q

Quick way to differentiate Mallory-Weiss syndrome from esophageal varices

A

Both will cause hematemesis, but Mallory-Weiss hematemesis is painful (b/c it’s a tear in the mucosa), while esophageal varices are painless bc/ veins have already ruptured

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20
Q

MC genetic translocation seen in leukemias

(a) B-ALL
(b) Acute promyelocytic leukemia
(c) CML

A

MC genetic translocation seen in

(a) B-ALL = t(12,21)
- 21: hence association w/ Down syndrome
(b) APL: t(15,17) that disrupts retinoic acid receptor needed for promyelocytic maturation
(c) CML: t(9,22) = Philadelphia chromosome

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21
Q

What two areas need prophylactic chemotherapy in tx of B-ALL?

A

B-ALL has a very good prognosis, w/ an excellent response to chemo
-but the chemo can’t cross the BBB or the blood-testes barrier => CSF and scrotum need prophylactic chemo

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22
Q

Pathology behind achalasia

(a) Secondary infectious cause of achalasia

A

Achalasia is 2/2 damage to ganglion cells in the myenteric plexus, myenteric plexus located btwn the inner circular and outer longitudinal layers of the muscularis propria

(a) Mostly idiopathic, but achalasia can be 2/2 chagas disease (trypanosoma cruzi infxn)

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23
Q

How to differentiate the two types of ALL

A

ALL split into B-ALL and T-ALL, differentiate by cell markers
-but both tdt + (DNA polymerase in lymphoblasts)

B-ALL: CD10, CD19, CD30
T-ALL: CD2 to CD8 (no CD10)

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24
Q

What is Whipple disease?

(a) Cause
(b) Clinical presentation
(c) Systemic features

A

(a) Whipple disease = infection w/ Tropheryma whippelli organism- organism can’t be fully destroyed by macrophages => macrophages accumulate partially-destroyed organisms inside lysosomes and build up in the lamina propria (CT) of the gut
(b) Small bowel lamina propria (positive on PAS stain for organism) is inundated w/ macrophages, which block lacteals => chylomicrons can’t be absorbed => pts p/w fat malabsorption and steatorrhea
(c) Can also cause systemic tissue damage: arthritis, cardiac valves, LN, CNS

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25
Q

Differentiate the two subsets of lymphoma: NHL vs. HL

(a) MC?
(b) Creation of mass

A

Non Hodgkin Lymphoma vs. Hodgkin Lymphoma

(a) NHL 60%, HL only 40%
(b) NHL- the mass is all proliferated cells
While in HL rare neoplastic cells (Reed Sternberg cells) produce cytokines to draw in other cells, so the mass is almost all composed of the reactive inflammatory cells

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26
Q

Differentiate intestinal and diffuse type of gastric carcinoma

A

Intestinal type = large irregular ulcers on lesser curvature of the antrum
-RF: intestinal metaplasia (seen in chronic gastritis from H. pylori or autoimmune)

Diffuse type = signet ring cells, desmoplasia thickens stomach wall

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27
Q

Celiac disease

(a) Associated immunodeficiency
(b) Antibodies present

A

Celiac disease

(a) Associated w/ IgA deficiency => if high suspicion remember to also check for IgG antibodies against tissue transglutaminase
(b) Anti-tissue transglutaminase, anti-endomysium (lining of individual nerve fibers), or anti-gliaden

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28
Q

Where does the virus that causes oral herpes lay dormant?

A

HSV-1 (causes majority of oral herpes cases) lays dormant in the ganglia of the trigeminal nerve

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29
Q

Acute promyelocytic leukemia- go to treatment

A

APL is due to t(15,17) that disrupts retinoic acid receptor needed for promyelocytes to mature => for tx give ATRA (retinoic acid derivative) to decrease blast burden b/c cells can now mature

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30
Q

Differentiate the two causes of chronic gastritis

(a) Location
(b) MC
(c) Mechanism

A

Chronic gastritis:

(b) H. pylori MC (90% of cases)
(a) H. pylori inflammation MC involves the antrum (distal portion, closest to duodenum)
(c) H. pylori sits on top of epithelium (doesn’t invade) and releases ureases and proteases to weaken mucosal defenses

Autoimmune chronic gastritis: due to Ai destruction of gastric parietal cells

(a) Parietal cells concentrated in the fundus and body of the stomach
(c) Chronic inflammation causes intestinal metaplasia (intestinal mucosa w/ Peyer’s patches are more able to handle stress of inflammation). No more parietal cells => achlorhydria and megaloblastic (pernicious) anemia

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31
Q

Cancers associated with

(a) Eosinophilia
(b) Basophilia

A

Blood cancers seen w/

(a) Eosinophilia = Hodgin lymphoma
- 2/2 IL-5 production
(b) Basophilia = CML
- recall: overproduction of mature granulocytes, especially basophils

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32
Q

When does pyloric stenosis present?

A

Pyloric stenosis is NOT PRESENT AT BIRTH!! the pyloric muscle hypertorphy (for unknown reason) starts after birth) so pts present w/ non-bilious vomiting around 2 wks of life

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33
Q

2 factors that determine risk of carcinoma in pts w/ Ulcerative Colitis

A
  1. extend of colon disease
    - of course the more colon that is inflammed, higher the risk
  2. duration of disease
    - generally don’t get cancer w/o at least 10 yrs of disease
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34
Q

Name a cancer that can cause ectopic production of EPO

A

Renal cell carcinoma can produce EPO

=> can cause a hyperplastic (not neoplastic) proliferation of RBCs that may be hard to distinguish from polycythemia vera

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35
Q

Subclasses of AML

(a) Acute Promyelocytic Leukemia- MC cytogenetic abnormality
(b) Acute monocytic leukemia- how does this present?
(c) One seen in Downs syndrome pts before age 5

A

AML subsets

(a) APL: t(15,17) that disrupts retinoid acid receptor needed for promyelocyte maturation
(b) Acute monocytic leukemia presents w/ gum swelling b/c hte monoblasts infiltrate the gums
(c) Acute megakaryoblastic leukemia

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36
Q

Multiple myeloma

(a) Explain why you get bony lytic lesions
(b) Finding on serum protein electrophoresis

A

Multiple myeloma

(a) Plasma cells secrete osteoclast-activating factor => bony lytic lesions of vertebrae and skull and hypercalcemia
(b) M-spike due to monoclonal antibody production

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37
Q

Differentiate what would cause transmural vs. only mucosal infarction in the bowel

A

Transmural infarction due to arterial thrombosis/embolism (ex: AFib, vasculitis) or venous thrombosis (polycythemia vera)

While mucosal infarction (mucosa is farthest from blood supply) arises from low blood flow states like hypovolemia/shock

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38
Q

Explain a group of syndromes that can progress to AML

A

Myelodysplastic syndrome = neoplastic accumulation of mature cells in the myeloid lineage, so this can prgoress to neoplastic accumulation of immature cells w/ just a different mutation
-so neoplastic process of myeloid lineage but blasts are under 20%

= CML, P. vera, Essential thrombocytopenia

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39
Q

MC site of volvulus in

(a) Elderly
(b) Young adults

A

Volvulus most likely to develop in place w/ extra mesentery where it can twist on itself

(a) Elderly = sigmoid colon
(b) Cecum in young adults

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40
Q

Explain why H. pylori infection causes chronic gastritis

A

H. pylori sits on top of the gastric mucosa (doesn’t invade the mucosa itself) and releases proteases and urases that weaken mucosal defenses and cause inflammation

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41
Q

Explain why Meckel’s diverticulum may bleed (aka 2 yo p/w melena)

A

Meckel’s diverticulum often has heterotopic gastric tissue in it that produces H+ that breaks down intestinal wall => bleeds

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42
Q

LN spread of esophageal malignancy

(a) Upper 1/3
(b) Middle 1/3
(c) Lower 1/3

A

LN spread depends on where in the esophagus

(a) Upper 1/3 to cervical LN
- squamous cell carcinoma 2/2 irritation

(b) Middle 1/3 to mediastinal or tracheobronchial nodes

(c) Lower 1/3 to celiac and gastric nodes
- adenocarcinoma from Barret’s/GERD, b/c needs Barret’s or else there wouldn’t be glands in the esophagus to become cancerous

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43
Q

Differentiate leukemia and lymphoma

A

Both are neoplastic proliferation of cells from hematopoietic stem cell lines

Leukemia = when these cells stay in the blood

Lymphoma = when these cells form a mass (can be in LN or extranodal)

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44
Q

Describe the cardiac complication seen in carcinoid heart disease

(a) What kind of carcinoid tumors cause this?
(b) How to tell if pt will get R or L sided cardiac lesion?

A

Excess serotonin causes fibrosis of heart valves => right sided lesions such as TR

(a) Mets to liver, b/c venous drainage needs to bypass liver or else excess 5-HT is metabolized by MAO into 5-HIAA and excreted in urine and you don’t get the clinical syndrome
(b) Carcinoid syndrome CANNOT cause left sided heart lesion b/c lung contains MAO that will convert 5-HT into 5-HIAA so the fibrosis-stimulating 5-HT doesn’t reach the left heart

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45
Q

Differentiate Marginal Zone Lymphoma from Burkitt Lymphoma

(a) Cells
(b) Associated condition

A

Marginal Zone Lymphoma

(a) Neoplasia of small B cells
(b) Chronic inflammatory states: Hashimoto’s, H. pylori gastritis, Sjogrens

Burkitt Lymphoma

(a) Neoplasia of intermediate sized B cells
(b) EBV infection

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46
Q

Name two places where Burkitt Lymphoma typically present

(a) Molecular cause

A

Burkitt Lymphoma = neoplastic proliferation of intermediate sized B cells

Clasically presents with:

  • mass in jaw in African Americans
  • mass in abdomen in sporadic form

(a) C-myc translocation

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47
Q

Celiac disease vs. tropical sprue- name 2 ways to differentiate

A

Tropical sprue is when small bowel villi are damaged due to an unknown organism- but key differentiation is that it’s infectious

So topical sprue arises after infectious diarrhea and responds to abx
-also often occurs in tropical regions

Another big distinction = location

  • Celiac disease involves duodenum
  • Tropical sprue most prominent in jejunum and ileum
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48
Q

Which type of AML can be a medical emergency?

A

Acute promyelocytic leukemia can become a medical emergency
-promyelocytes have tons of Auer rods (crystal aggregates of MPO) which can activate the coagulation cascade and potentially cause DIC

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49
Q

Differentiate pleomorphic adenoma and mucoepidermoid carcinoma of the salivary glands

A

Pleomorphic adenoma = benign, both stromal and epithelial tissue, painless (b/c hasn’t invaded facial nerve b/c benign)

Mucoepidermoid carcinoma = malignant, both mucinous and squamous cells, usually of parotid, commonly involves facial nerve (so facial palsy/pain)

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50
Q

Name the 3 features of carcinoid syndrome

A

2/2 excess 5-HT (serotonin) release

  1. bronchospasm
  2. diarrhea
  3. flushing of skin
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51
Q

Classic cause of dysphagia to BOTH liquid and solid

A

When you can’t swallow liquids too (and not progressive as in it started w/ solids and now it’s both) think achalasia = esophageal dysmotility and inability of LES to relax

B/c need esophageal peristalsis and relaxed LES to let liquids into stomach too

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52
Q

Differentiate erosion from ulceration

A

First recall layers of the GI tract: mucosa –> submucosa –> muscularis propria –> serosa

Erosion = involves only mucosa (heals w/ full resolution)

Ulceration = extends into submucosa (heals w/ fibrosis/scaring)

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53
Q

Bacteria that causes lymphocytic (instead of neutrophilic) leukocytosis

A

Bordetella pertusis- bacteria that causes lymphocytic leukocytosis (usually seen in viral infections)

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54
Q

Which blood cancer do you think first when a teenager presents w/ a mediastinal/thymic mass?

A

T-ALL = acute lymphoblastic lymphoma

lymphoma and not leukemia b/c the T cells aren’t in the blood, they’re making a mass in the thymus

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55
Q

Celiac disease

(a) Type of hypersensitivity
(b) Pathogenic antigen
(c) Associated derm finding

A

Celiac disease

(a) Type IV hypersensitivity b/c delayed T-cell response
(b) Gliaden is the part of gluten that is pathogenic
(c) Dermatitis herpetiform- IgA deposition at tip of dermal papillae cause small grouped vesicles that looks like (but has nothing to do with) herpes

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56
Q

Which region of the lymph node would be enlarged due to

(a) RA
(b) Early HIV
(c) Viral infection
(d) Reactive LN = LN draining cancerous tissue

A

(a, b) RA and early HIV cause hyperplasia in the follicular region

  • chronic inflammatory cells (for RA), and follicular cells are CD4+ (early HIV)
    (c) Viral infection causes expansion of paracortex (where the T cells are)
    (d) LN draining cancerous tissue undergo hyperplasia of the sinus histiocytes (deep in the medulla)
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57
Q

Differentiate Sister Mary Joseph nodule and Krukenberg tumor

A

Sister Mary Joseph nodule = periumbilical nodule indicative of underlying malignancy

  • usually gastric adenocarcinoma metastasized to the liver
  • seen in intestinal type gastric adenocarcinoma

Krukenberg tumor = b/l ovarian metastasis from gastric carcinoma
-seen in diffuse type gastric adenocarcinoma

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58
Q

Differentiate the toxin in acute vs. chronic gastritis

A

Acute gastritis = breakdown of stomach wall from either too much acid or breakdown of mucosal barrier

Chronic gastritis from chronic inflammation- MC from H. pylori, also from autoimmune destruction

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59
Q

MC primary malignancy of bone

(a) Involved IL

A

Multiple myeloma = MC primary malignancy of bone

(a) IL-6

60
Q

Adult onset asthma- buzzword for what dx?

A

Adult onset asthma- first r/o GERD

61
Q

Esophageal web- buzzword for what dx?

A

Esophageal web = thin protrusion of esophageal mucosa that can cause partial obstruction

Buzzword for Plummer-Vinson syndrome

62
Q

Myeloproliferative d/o of

(a) granulocytes
(b) Erythroblasts
(c) Megakaryoblast
(d) Plts

A

Myeloproliferative d/o = neoplastic proliferation of mature cells of the myeloid lineage

(a) Granulocytes, especially basophils = CML
(b) Erythroblasts = Polycythemia vera
(c) Megakaryoblasts = Myelofibrosis
2/2 oversecretion of PDGF
(d) Plts = Essential thrombocytopenia

63
Q

What are Auer rods?

(a) Seen in what?

A

Auer rods = crystal aggregates of MPO

(a) Seen in AML = acute myeloblastic leukemias

64
Q

Differentiate the two precursor lesions to squamous cell carcinoma of the mouth

A

Precursor lesions = leukoplakia (white plaque, not scraped away like candida) and erythroplakia (red plaque b/c vascularized)

-don’t confuse this w/ hairy leukoplakia, which is NOT pre-malignant

65
Q

Which chronic leukemia presents similarly to multiple myeloma

A

ATLL (Adult T cell Leukemia Lymphoma) = neoplastic proliferation of mature CD4+ T cells
-associated w/ HTLV-1 (Japan and Caribbean)
presents w/ lytic bone lesions and hypercalcemia (similar as MM)

But ATLL will have a rash (b/c CD4+ T cell proliferation => rash), while MM has no rash

66
Q

Definition of acute leukemia

(a) How does this clinically present

A

Acute leukemia = neoplastic proliferation of immature blood cells (blasts) making up 20% or more of bone marrow

(a) Blasts crowd out bone marrow, so pt presents due to decrease in the other cell lines
- anemia
- leukopenia
- thrombocytopenia

67
Q

What is Marginal Zone Lymphoma?

(a) Seen in what conditions?
(b) Tx for this in the gut

A

Marginal Zone is created from B cells from the germinal centers => need to be creating lots of inflam. response for this zone to proliferate

(a) Seen in chronic inflammatory states: Hashimotos, Sjogrens, H. pylori gastritis
(b) In the gut this can cause MALT, which can regress w/ H. Pylori eradication

68
Q

Explain the clinical presentation of pts w/ lactose intolerance

A

Lactose enzyme not available to break down lactose into galactose and glucose => lactose remains in intestinal lumen and acts as osmotic diuretic => watery diarrhea

69
Q

Infectious Mononucleosis

(a) Less common cause
(b) Part of spleen that enlarges
(c) Definitive test

A

Infectious Mono

(a) Usually by EBV, less commonly caused by CMV
- suspect CMV if monospot test is still negative after first week
(b) Periarterial lymphatic sheath of the white pul expands
(c) After positive monospot screening test, dx definitively w/ EBV viral capsid antigen

70
Q

Blood cancer increased risk in Downs syndrome pts

(a) before age 5
(b) after age 5

A

Downs syndrome pts have an icnreased risk of malignancy

(a) Before age 5- Acute Megakaryoblastic leukemia = neoplastic proliferation of megakaryoblasts
- lack MPO

(b) After age 5- ALL (acute lymphoblastic leukemia)
- so acute leukemia (blasts over 20%) due to accumulation of lymphoblasts (lymphoblastic lineage- so split into T-ALL and B-ALL

71
Q

Explain the following consequences of multiple myeloma

(a) Increased infection risk
(b) Rouleux formation
(c) Risk of which type of amyloidosis?
(d) Bence-Jones proteins

A

Multiple myeloma

(a) Decreased variability in cell immunity => increased risk of infection
(b) Rouleux formation of RBCs (stacks formed) b/c the increase in serum protein decreases the charges btwn RBCs
(c) Increased risk of AL amyloidosis 2/2 massive increase in IgL (immunoglobulin light chain)
(d) Bence-Jones = Ig light chain found in urine

72
Q

Super random but what blood type is a risk factor for a certain GI cancer?

A

Blood type A is a risk factor for intestinal-type gastric carcinoma

73
Q

Triple therapy for H. pylori eradication

A

PPI, amoxicillin, clarithromycin

74
Q

Mutation implicated in most myeloproliferative d/o

A

JAK2-kinase mutation

-associated w/ polycythemia vera, essential thrombocytopenia, and myelofibrosis

75
Q

Leser-Trelat sign

A

Leser-Trelat sign = acute onset of tons of seborrheic keratoses (‘stuck-on’ dark lesions) = indicative of underlying cancer
-usually underlying gastric adenocarcinoma

76
Q

Biopsy finding in duodenal ulcers

A

Duodenal ulcers- see hypertrophy of Brunner’s glands (mucus-secreting glands)

77
Q

Differentiate Curling and Cushing ulcers

A

Curling ulcer = ulcer due to severe burns causing hypovolemia. Hypovolemia => reduced blood flow to Gi tract so reduced removal of acid and reduced nutrients to barrier

Cushing ulcer = elevated ICP causes direct stimulation of vagus nerve, vagal stimulation secretes ACh that directly stimulates parietal cells into fundus and body of stomach to release more acid

78
Q

Translocations seen in the small cell Non Hodgkins Lymphoma

(a) Follicular lymphoma
(b) Mantle cell lymphoma

A

Translocations

(a) Follicular lymphoma: t(14,18)
- Bcl2 w/ IgH, Bcl2 is needed to stabilize mitochondrial membrane and prevent apoptosis, but in these B cells undergoing somatic hypermutation apoptosis is needed => this translocation prevents B cells in the follicles from undergoing apoptosis as Bcl2 keeps c-myc in the mitochondria (and therefore unable to activate capsases)
(b) Mantle cell lymphoma: t(11,14)
- Cyclin D1 (cell cycle regulator, G1 –> S) w/ IgH (immunoglobulin heavy chain)

79
Q

Which artery causes bleeding 2/2

(a) Rupture of posterior duodenal ulcer
(b) Rupture of gastric ulcer

A

(a) Posterior duodenal ulcer ruptures and causes bleeding from gastroduodenal artery (runs on the posterior border of the duodenum)
(b) While gastric ulcers are MC located on the lesser curvature of the antrum, where the left gastric artery runs

80
Q

MC cause of appendicitis in children vs. adults

A

Children- lymphoid hyperplasia

Adults- fecolith (just a piece of fecal material) obstruction

81
Q

Classic clinical presentation (including demographics) of IBD vs. IBS

A

IBD = young women (30s) w/ recurrent bouts of bloody diarrhea and abdominal pain

  • diagnosis of exclusion
  • subclassified into Crohns and UC

IBS = relapsing abdominal pain and change in bowel habits that improves w/ defecation, classically middle aged females
-biopsy normal

82
Q

Explain what type of biopsy is needed to dx Hirschsprung disease

A

Need to do suction biopsy, can’t just do regular biopsy

Regular biopsy will only give mucosa, while you need to get into the muscularis propria to see if the nerve plexi are missing to dx Hirschsprung

83
Q

UC vs Crohn

(a) Full thickness
(b) Knife-like fissures vs. ulcers
(c) LLQ pain
(d) RLQ pain

A

(a) Crohns has full thickness lesions
- ulcers are defined as only mucosa and a bit of submucosa

(b) Knife-like fissures in Crohns b/c full thickness
(c) LLQ pain in UC b/c rectum then ascends (on left side)
(c) RLQ pain in Crohns b/c MC involves terminal ileum

84
Q

UC vs Crohn

(a) Associated w/ PSC
(b) Effect of smoking

A

(a) UC associated w/ PSC
(b) Smoking is ironically protective against UC, but is a rsk factor for Crohns
- stupid, obv don’t smoke anyway, but know that ironically smoking is protective against UC

85
Q

Describe what specific points in the colonic wall are weakest => most susceptible to diverticula

A

Diverticula develop right where vasa recta (veins) transverse the muscularis propria
-b/c diverticula are outpouches of mucosa and submucosa thru the muscularis, so makes sense that they’d go where something else (the veins) are already making a hole)

86
Q

2 main manifestations of Hereditary Hemorrhagic Telangiectasias

A

HHT: autosomal dominant d/o causing thin-walled blood vessels, especially in the

  1. mouth (get telangiectasias on lips)
  2. GI tract => presents w/ GI bleed
87
Q

MC cause of ischemic colitis

(a) MC location involved

A

MC cause of ischemic colitis = atherosclerosis of the SMA

(a) Splenic flexure = SMA watershed region

88
Q

Clinical presentation of ischemic colitis

A

Post-prandial abdominal pain

-b/c w/ meals you increase O2 demand, which can’t be met by atherosclerotically narrowed vessel

89
Q

Explain how aspirin is thought to be protective from adenoma-carcinoma sequence

A

In the 3rd step of the vogelgram (APC –> kRAS –> p53) you also see increase in COX expression to allow polyp to progress to carcinoma

-aspirin is a COX inhibitor => aspirin works on third step to impede progression of adenoma to carcinoma

90
Q

Name the 3 steps of the vogelgram and how they fit into adenoma-carcinoma sequence seen in CRC

A
  1. APC mutation- creates the risk for polyp formation
  2. kRAS mutation- actual polyp formation
  3. p53 mutation- transformation of adenomatous polyp into carcinoma
    - also have increased COX expression here
91
Q

Polyps w/ greater risk of progression to carcinoma

(a) Size cutoff
(b) Sessile vs. pedunculated
(c) Tubular vs. villous

A

CRC adenoma to carcinoma sequence

(a) Greater than 2 cm
(b) Sessile has higher risk of progression
- think it’s easier to grow off a little stalk then horizontally on tissue (more contact w/ tissue)

(c) “villous is villain”- greater risk of progression from villous than tubular histology

92
Q

Differentiate Gardner and Turcot syndrome

A

Both Gardner and Turcot syndrome are FAP (familial adenomatous polyposis- APC mutation on chromosome 5) variants w/ additional tumors

Gardner = FAP w/ fibromatosis (soft tissue tumors) and osteomas

Turcot = FAP w/ CNS tumors

93
Q

What is Peutz-Jeghers syndrome?

A

Aut dominant d/o of hamartomatous (benign) polyps of the skin and GI tract

-huge increased risk of CRC

94
Q

2 other cancers (besides CRC) that pts w/ HNPCC are at increased risk of

A

HNPCC = cancer syndrome 2/2 mutation in mismatch repair enzyme, leading to microsatellite instability

Increased risk of CRC, ovarian, and endometrial cancer

95
Q

Differentiate the colonic carcinomas seen in HNPCC vs. FAP

A

FAP = APC mutation, so these cancers start as polyps and undergo adenoma-carcinoma sequence (APC, kRAS, then p53 mutation)

While HNPCC tumors arrive denovo (b/c mismatch repair enzyme mutated), not from polyps
-more commonly right sided

96
Q

Currant jelly stools

A

Buzzword for intussusception

97
Q

Differentiation clinical presentation of achondroplasia and osteogenesis imperfecta

A

Achondroplasia (impaired cartilage growth) => dwarfism
-short b/c long bones grow via endochondrial formation (on cartilage matrix) while skull and rib cage (unaffected) grow by intramembranous formation (w/o preexisting cartilage formation)

Osteogenesis imperfecta (defect in collagen I) => impaired bone formation => multiple fractures, blue sclera, hearing loss

98
Q

Mutation causing achondroplasia

A

Activating mutation in fibroblast growth factor that inhibits growth => impaired cartilage growth

99
Q

Explain blue sclera finding in osteogenesis imperfecta

A

OI => blue sclera b/c defect in collagen I exposes the choroidal veins that lie behind the thinned sclera

100
Q

Explain the pathogenesis that causes osteopetrosis

A

Osteopetrosis = defect of bone resorption causing thick, heavy bone that easily fractures

MC caused by mutation in carbonic anhydrase II => can’t make the acidic environment needed to remove Ca2+ from bone
Recall: need acid (carbonic anhydrase) to remove Ca2+ from bone, need alkaline environment to build bone (hence why alk phos released when osteoblasts are activated)

101
Q

Explain these findings of osteopetrosis

(a) Hearing impairment
(b) Renal tubular acidosis
(c) Anemia

A

Osteopetrosis = defect in bone resorption 2/2 mutation in carbonic anhydrase impairing acidic environment needed for bone breakdown
Bone can’t be broken down => bone gets super thick and heavy

(a) Hearing and visual impairments are bone thickens and impinges cranial nerves
(b) RTA b/c w/o carbonic anhydrase, can’t break down H2CO3 –> H+ (out in urine) for HCO3- to be taken back into body
(c) Anemia b/c bone marrow replaced by expanding bone/cortex

102
Q

Tx for

(a) Achondroplasia
(b) Osteopetrosis

A

(a) Achondroplasia = dwarfism but mental fxn life span and fertility are unaffected => no tx

(b) Osteopetrosis = can’t break down bone due to carbonic anhydrase mutation (can’t make acidic environment for osteclasts to work in)
- tx w/ bone marrow transplant: new osteoclasts (w/ functioning carbonic anhydrase) prodcued from new monocytes

103
Q

Effect of vitamin D deficiency in children vs. adults

A

Vit D deficiency in children => Rickets
-pigeon breast deformity, frontal bossing, rachitic rosary, bowing of legs

Vit D deficiency in adults => osteomalacia
-increased risk of fracture

104
Q

70 yo F fractures a bone- easy way to distinguish osteomalacia from osteoporosis

A

Osteomalacia (weak bones 2/2 vitamin D deficiency) vs. osteoporosis (reduction in trebecular bone mass) differentiated by simple lab test

Osteomalacia: low serum calcium and phosphate, elevated PTH and alk phos

Osteoporosis: normal labs!

105
Q

Paget disease

(a) Buzzword clinical presentation
(b) Unique lab finding

A

Paget disease = imbalance btwn osteoclast and osteoblast activity => abnormal deposition of bone

(a) Increasing hat size 2/2 skull enlargement
(b) Isolated elevation in alk phos
- no mineral abnormalities (normal Ca Phos)
- but osteoblasts are active => alk phos elevated

106
Q

2 complications of Paget disease of bone

A

Paget disease of bone = imbalance btwn osteoclast and osteoblasts leading to abnormal irregular bone deposition

2 complications

  1. osteosarcoma = malignant tumor of osteoblast
  2. high output heart failure: b/c AV shunts form in bone that heart has to push thru
107
Q

Tx for Paget disease of bone

A

Paget disease of bone = imbalance of osteoclast vs. osteoblast activity causing deposition of abnormal irregular bone

Tx = calcitonin (inhibits osteoclast fxn so stop chewing down bone)
Bisphosphonates: induces apoptosis of osteoclasts

108
Q

Differentiate location of osteomyelitis in children vs. adults

A

Osteomyelitis: infection of marrow and bone via hematogenous spread

  • transient bacteremia in children seeds metaphysis (growth plate)
  • open wound bacteremia in adults seeds epiphysis (above metaphysis)
109
Q

Expected cause of osteomyelitis in

(a) Diabetics
(b) Sickle cell disease
(c) Sexually active young adult
(d) Cat/dog bite
(e) Overall MC cause

A

(a) Diabetes and IVDU- pseudomonas
(b) SCD- salmonella
(c) Sexually active young adult- Neisseria gonorrhea
(d) Cat/dog bite- pasteurella
(e) Overall, 90% cases caused by S. aureus

110
Q

Differentiate osteoid osteoma and osteoblastoma

A

Both are benign tumors of bone

Osteoid osteoma: smaller (under 2cm), arises in cortex, bone pain that is relieved by aspirin

Osteoblastoma: larger (over 2cm), arises in vertebrae, pain NOT relieved by aspirin

111
Q

Bone tumor that arises from the

(a) Metaphysis
(b) Epiphysis

A

(a) Osteosarcoma = malignant tumor of osteoblasts that arises in the metaphysis of long bones
(b) Giant cell tumor = in young adults, arises in the epiphysis of long bones

112
Q

Ewing sarcoma

(a) Derived from what tissue?
(b) Xray appearance
(c) Where does it arise?

A

Ewing sarcoma = bone tumor in child 2/2 t(11;22)

(a) Derived from neuroectoderm
(b) Onion skin appearance on Xray
(c) Arises at diaphysis (shaft) of long bone, usually in males under 15

113
Q

Ewing sarcoma- how to differentiate from lymphoma

A

Both Ewing sarcoma and lymphoma may present as acutely inflammed joint w/ fever

Ewing sarcoma cells: small, round blue cells that resemble lymphocytes, will have t(11;12)

Translocation of 11;22 = characteristic for Ewing Sarcoma

114
Q

Differentiate location of chondroma and chondrosarcoma

A

-cartilage tumors arise from the medulla

Chondroma = benign tumor of cartilage, arises in medulla of small bones of hands and feet (ex: fingers)

Chondrosarcoma = malignant tumor of cartilage, again arises in medulla but this time in pelvis or central skeleton

115
Q

Appearance of mets to bone

A

Metastatic tumors to bone are primarily osteolytic (punched out) lesions

One exception = prostate carcinoma- forms osteoblastic lesion

116
Q

Explain the different clinical picture of osteoarthritis and RA

A

OA: stiffness in morning that worsens throughout the day (b/c worsens w/ use!)

RA: morning stiffness improves w/ activity b/c diffusing/moving around the inflammatory cells

117
Q

Hallmark tissue found in rheumatoid arthritis

A

Pannus = inflamed granulation tissue in the synovium = hallmark of RA

118
Q

Differentiate joints involved in OA vs. RA

A

OA: both DIP (Heberden nodes) and PIP (Bouchard nodes)

RA: PIP, but DIP usually spared!!!

119
Q

2 complications of the chronic inflammation seen in RA

A
  1. Anemia of chronic disease from increase in hepcidin (acute phasereactant)
  2. Upregulate acute phase reactant SAA, SAA converted into AA that deposits in tissues => secondary amyloidosis
120
Q

Name the triad seen in Reiter syndrome (seronegative spondyloarthropathies)

A

Reiter syndrome = arthritis, urethritis, and conjunctivitis

“can’t see, can’t pee, and can’t climb a tree”

Seronegative b/c negative rheumatoid factor

121
Q

Explain increased risk of gout in Lesch-Nyhan syndrome

A

Lesch-Nyhan syndrome = X-linked deficiency in HGPRT which is used to recycle hypoxanthine and guanine so they don’t get shunted to uric acid.

W/o HGPRT hypoxanthine and guanine (therefore AMP and GMP, their precursors respectively) are all made into uric acid => excess uric acid precipitates in joints = gout

122
Q

Positive ANA w/ malar rash

(a) w/ anti-dsDNA Ab
(b) W/ anti-Jo1 ab

A

(a) Lupus

(b) Dermatomyositis

123
Q

How to differentiate dermatomyositis and polymyositis

A

Besides absence of skin findings in polymyositis, can do muscle biopsy:

Dematomyositis: perimysial (periphery of muscle fiber) infalmmation

Polymyositis: enodmysial inflammation

124
Q

One surgery that can improve symptoms of myasthenia gravis

A

Thymectomy b/c associated w/ thymic hyperplasia or thymoma

125
Q

Grape-like mass protruding from vagina of 5 yo that stains desmin positive

A

Desmin positive stain characteristic of muscle, mass in vagina is classic site of rhabdomyosarcoma (malignant tumor of skeletal muscle)
-MC site overall is head and neck

126
Q

HPV serotypes

(a) Condyloma acuminatum
(b) Squamous cell carcinoma

A

(a) Condyloma acuminatum associated w/ HPV type 6 and 11 (low risk)

(b) SCC associated w/ high risk HPV types 16, 18, 31, 33
- explains how lack of circumcision may pose increased risk of penile cancer b/c foreskin acts as nidus for inflammation and irritation

127
Q

(a) MC congenital male reproductive abnormality
(b) MC testicular tumor
(c) MC testicular tumor in children

A

(a) Cryptorchidism = failure of testicle to descend into scrotal sac

(b) MC testicular tumor = germ cell tumor (95%)
- most are mixed germ cell tumors

(c) MC testicular tumor in children = yolk sac (endodermal sinus) tumor
- subtype of non-seminoma germ cell tumor

128
Q

Indication for orchiopexy

A

Orchiopexy = surgically move down undescended testes (to treat cryptorchidism)

  • most will spontaneously regress, so only do the surgery if male is almost 2 and it hasn’t descended
  • do before age 2 b/c can be associated w/ testicular atrophy/infertility b/c testicles need colder temp of outside than body temp
129
Q

Ddx for granulomas in the seminiferous tubules

A

Ddx = Tb and autoimmune orchitis (orchitis = testicular inflammation)

Differentiate by AFB

130
Q

MC cause of prostatitis and orchitis

A

Separated by age group

Young sexually active males = N. gonorrhea and chlamydia trachomatis

Older adults see spread of UTI infxns to reproductive tract = E. Coli and Pseudomonas

131
Q

Type of infarction seen in testicular torsion

A

Hemorrhagic infarction (not ischemic) b/c the torsion first obstructs the vein (collapsible structure) => arterial blood flow enters dead tissue causing hemorrhage

132
Q

Differentiate varicocele and hydrocele

A

Varicocele = dilation of spermatic vein due to impaired lymphatic drainage (obstruction!)

Hydrocele = fluid collection in the tunica vaginalis (scrotal sac)

133
Q

Malignancy associated w/ varicocele

A

Varicocele = dilation of spermatic vein (palpate ‘bag of worms’ on physical exam)

L. varicocele can be due to obstruction of left renal vein (which indirectly then drains blood into IVC), renal cell carcinoma classically spreads to left renal vein

=> L. varicocele associated w/ L. RCC

134
Q

Varicocele more commonly left or right sided?

A

Left sided b/c left scrotal vein drains indirectly into IVC via the left renal vein, while right scrotal vein drains directly into IVC

135
Q

How to differentiate hydrocele from malignant process?

A

Hydrocele = fluid in the scrotum => can be transilluminated

While testicular tumor

136
Q

How to diagnose testicular tumors

A

DONT BIOPSY! Risk of seeding to the scrotum, and 95% are germ cell tumors anyway which are malignant => just do radical orchiectomy w/o biopsy

137
Q

Germ cell tumors: seminoma vs. non-seminoma

(a) Gross appearance
(b) Prognosis

A

Seminoma (resemble spermatogonia)

(a) Homogenous non-hemorrhagic non-necrotic mass
(b) Highly responsive to radiotherapy, metastasize late, excellent prognosis

Non-seminoma (not spermatogonia like) = embronal carcinoma, yolk sac tumor, choriocarcinoma, teratoma

(a) Hemorrhagic mass w/ necrosis
(b) Variable response to tx and often met early => worse prognosis

138
Q

Teratoma: M vs. F

A

Teratomas in females are benign, while they are malignant in males

Recall: teratoma = tumor composed of mature fetal tissue from 2-3 embryonic layers (at least 2 embryonic layers)

139
Q

Cause of hydrocele in adults vs. children

A

Hydrocele = fluid collection in the tunica vaginalis (scrotal sac)

In children 2/2 incomplete closure of the processes vaginalis, leading to communication w/ the peritoneal cavity

Caused by blockage of lymphatic drainage in adults

140
Q

DRE findings seen in

(a) Acute prostatitis
(b) BPH
(c) Potential prostatic adenocarcinoma

A

Digital rectal exam

(a) Acute prostatitis- feel tender and boggy prostate
(b) BPH- diffusely enlarged
(c) Irregular mass on posterior peripheral surface

141
Q

Dx acute and chronic prostatitis

A

Can dx by WBC in prostatic secretions

Can culture prostatic secretions- will see bacteria in acute, probs wont grow any bacteria in chronic

142
Q

Briefly describe the Gleason grading system for staging prostate cancer

A

Gleason grading system- graded on architecture alone, NOT nuclear atypia

So grading is unique in that multiple regions are assessed for architecture, while nuclear atypia is not included in the grading

143
Q

MC location of prostatic cancer mets

(a) Type of lesion seen

A

MC location of prostate mets = lumbar spine (p/w lower back pain) and pelvis

(a) Osteoblastic lesion
- key here b/c most mets present as osteolytic (punched out) lesions, but not prostate!!

144
Q

Clinical presentation of metastatic prostate cancer

(a) Lab findings

A

MC spreads to lumbar spine or pelvis => presents w/ lower back pain

(a) Elevated alk phos, PSA, and prostatic acid phosphate

145
Q

Medical vs. surgical tx for prostate cancer

A

If prostate cancer is localized do prostatectomy

Advanced disease: tx w/ hormone suppression to reduce DHT

  • Leuprolide = continuous GnRH analogue
  • Flutamide = competitive inhibitor of androgen receptor
146
Q

Compare the two medical tx for BPH

A

Treating BPH

  1. Alpha1 antagonist (terazosin) to relax smooth muslce
    - can also help lower BP
    - more immediate result but need to take everyday
  2. 5alpha reductase inhibitor: reduces conversion of T –> DHT => reduced stimulation on stromal epithelium
    - but takes months to have effect b/c actually works to shrink the prostate
    - also can be used for male pattern baldness
    - side effects may be gynecomastia and sexual dysfunction
147
Q

PSA levels

(a) Normal
(b) BPH
(c) Concerning for cancer

A

PSA = prostate-specific antigen, produced by prostate glands to liquefy semen

(a) Normal is under 4 ng/mL
(b) BPH shows slight elevation of 4-10, b/c more glands = more PSA produced
(c) Normal PSA increases w/ age, normal can be up to 7.5 for males in their 70s, but anything over 10 is worrisome for cancer at any age

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