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PATH FINAL > Body PATH > Flashcards

Body PATH Flashcards

1
Q

Polyarteritis Nodosa (PAN)
- Epi
- Affected parts ?
- Association ?
- Prognosis ?

A

Epi
- PAN is more common in MAN

Affects
- Renal (90% - microaneurysms), GI, Cardiac, CNS (aneurysms)
- spares Lung

Associations
- Hep B and C**

Prognosis
- Fatal if untreated (progressive renal failure or gastrointestinal complications)

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2
Q

PAN patho

A

PAN: Immune complex mediated

Wegners, Churg Strauss, Microscopic Polyangiitis: ANCA

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3
Q

Churg Strauss
- Association
- Features

A

Association
- Eosinophilic lung disease + Asthma

Feature
- Transient peripheral lung consolidation (if cavitation think Wegners)

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4
Q

HSP
- features

A

Most common vasculitis in Children
Systemic disease (GI most common)

Feature
- Painful bloody diarrhea
- Common lead point for Intuss
1) Intussusception
2) Scrotum with massive skin oedema
3) Colitis (thumb printing on x-ray)

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5
Q

Behcets
- Clinical presentation ?
- Feature

A

Clinical
- Mouth and genital ulcers
- Turkish descent
- Aortic thickening

Feature
- Pulmonary artery aneurysm (likely shown)*
- pericarditis
- CNS: T2 hyperintensities (thalamus, midbrain, and internal capsule): most common

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6
Q

Congenital Hypertrophic Pyloric Stenosis
- RF

A
  • Twins: Monozygotic (higher risk)
  • Trisomy 18, Turners
  • Erythromycin or azithromycin exposure, either orally or via mother’s milk
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7
Q

Hirschprung disease
- Mutated gene

A
  • RET account for the majority of familial and
    approximately 15% of sporadic
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8
Q

Hirschprung disease
- Associations

A
  • Down syndrome (10%)
  • Serious neurological disease
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9
Q

Esophageal web
- location
- association

A

Location
- Upper esophagus

Association
- Plummer-Vinson syndrome: iron deficiency anemia, glossitis, and cheilosis
- graft-versus-host disease
- gastro-oesophageal reflux disease
- Radiation

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10
Q

Esophageal web
- Circumferential or Semi-circumferential

A
  • Semi-circumferential (typically arise from the anterior wall and never from the posterior wall)*
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11
Q

Zenkers Diverticulum vs Killian-Jamieson location

A

Zenkers
- Hypopharynx (not cervical esophagus)
- Posterior
- Pulsion type

Killian-Jamieson
- Cervical esophagus (below cricopharyngeus)
- Anterolateral

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12
Q

Epiphrenic Diverticula vs Para-esophageal hernia location

A

Epiphrenic Diverticula
- just above the Diaphragm (usually right)
- pulsion type

Para-esophageal hernia
- on the left
- pulsion type

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13
Q

Barrett esophagus
- Metaplasia of what to what ?
- Increased risk for ?

A

Cause
- Intestinal (Columnar) metaplasia of esophageal squamous epithelium

Increased risk
- 40x increased risk for adenocarcinoma* (10% progresses to adenocarcinoma*)

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14
Q

Barrett esophagus
- Microscopic finding

A
  • Goblet cells (diagnostic), secrets mucin
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15
Q

Barrett Esophagus stricture at high, mid or low esophagus ?

A

Mid esophagus

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16
Q

Carcinoid
- risk factors

A
  • Autoimmune chronic gastritis
  • MEN-1
  • NF-1 (gist also NF-1 RF)
  • TS
  • VHL
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17
Q

How common is Carcinoid syndrome

A
  • Uncommon (<10%)
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18
Q

Other syndrome Carcinoid can cause ?

A

Zollinger Ellison

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19
Q

Mesenteric Carcinoid more commonly a primary or metastatic deposit

A

Metastatic deposit from elsewhere

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20
Q

What can one measure for Carcinoid tumor

A
  • 24 hour urine 5-HIAA (metabolite of serotonin)
  • Chromogranin-A
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21
Q

What are the antibodies found in Celiac disease

A
  • transglutaminate IgA antibodies (most sensitive), antigliadin IgA or IgG, and anti-endomysial antibodies.
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22
Q

Right vs Left clinical symptoms of Colon cancer

A

Caecal and right-sided colon cancers: Fatigue and weakness due to iron-deficiency anaemia.

Left-sided: Occult bleeding, changes in bowel habits.

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23
Q

Explain the classic adenoma-carcinoma sequence

A

Accounts for up to 80% of sporadic colon tumours ie. Majority arise from polyps (1st path way, the other pathway is Microsatellite instability pathway)

  • “First hit” is either sporadic or inherited mutation of the APC allele followed by loss of the intact second
    copy of APC which is the second hit.
  • Further mutations of KRAS or inactivation of p53 accumulate then lead to the development of carcinoma.
  • Lose capacity to degrade B-catenin -> B-catenin accumulates -> Triggers cell proliferation

** KRAS gene is part of the signalling pathway that regulates cell growth

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24
Q

Ascending vs Descending colon cancer macroscopy

A

Ascending colon:
- Polypoid, exophytic masses, may be ulcerated
- Rarely obstruct

Descending colon:
- Annular lesions and cause luminal narrowing.
- Most are well to moderately differentiated adenocarcinomas with varying degrees of glandular differentiation and mucus production.

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25
Q

Menetrier disease involvement which part of stomach

A
  • Involves Fundus, spares Antrum
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26
Q

How does Pancreatic cancer cause Gastric Varices ?

A
  • Splenic vein thrombosis –> Gastric varices
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27
Q

All findings in Crohn’s

A
  • Cobble stone
  • Creeping fat
  • Crypt abscesses (UC also gets this)
  • Non-caseating granulomas
  • Pseudopolyps
  • Transmural with Lymphoid aggregates (UC has NO mural thickening - serosal surface normal)
  • Enlarged nodes (UC no enlarged nodes)
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28
Q

What are the 2 types of gastric cancer

A

Intestinal
- Preceded by Intestinal metaplasia*
- Bulky mass
- Form Glands*
- Broad cohesive fronts
- “neoplastic cells often contain apical mucin vacuoles”
- APC loss of function and gain of b-catenin function (c.f. Diffuse type)

Diffuse
- NO preceding intestinal metaplasia*
- Infiltrative
- Signet ring cell
- Don’t form glands
- Loss of e-cadherin (c.f. Intestinal type APC and b-catenin)
- Desmoplastic reaction*

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29
Q

Most common location of Gastric cancer in stomach

A
  • Lesser curve, Antrum*
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30
Q

Risk factors for GIT lymphoma

A

H-pylori (chronic inflammation) -> MALtoma - indoldent marginal B-cell lymphoma (ANTRUM)

Celiac disease -> T-cell lymphoma in proximal small bowel

Immunodeficiency, AIDS

Mediterranean lymphoma: Background of mucosal plasmacytosis

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31
Q

Causes of Chronic Gastritis

A

H-Pylori

Autoimmune Gastritis (Pernicious anemia)

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32
Q

Juvenile polyps
- associations
- Morphology

A
  • Sporadic (no malignant potential)
  • Syndromic (Malignant potential of colonic adenocarcinoma)
  • Have association with pulmonary AVMs.

Morphology
- characteristic cystic spaces representing dilated glands filled with mucin and inflammatory debris.

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33
Q

Peutz-Jeghers Syndrome
- associations

A
  • Cervical cancer (adenoma malignum)
  • Breast (50%)
  • Pancreas (36%)
  • Uterine, Ovary, Testis cancer
  • Lung
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34
Q

FAP mostly inherited or sporadic ?

A

Inherited (75%)

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35
Q

Gardner syndrome consists of ?

A
  • Osteomas
  • Desmoids tumours
  • Epidermoid cysts
  • Dental abnormalities
  • Hypertrophy of the retinal pigment epithelium
  • Follicular thyroid carcinoma
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36
Q

Most common syndromic form of colon cancer ?

A

HNPCC

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37
Q

HNPCC more common which side ?

A

Right side

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38
Q

HNPCC inheritance ?

A

AD
- MSH2 and MSH1

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39
Q

HNPCC increased risk for what cancers ?

A
  • Endometrium
  • Stomach
  • Ovary
  • Uterus
  • Brain
  • Small bowel
  • Biliary tract
  • Pancreas
  • Skin
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40
Q

Which phase of Ischemic bowel does the msot damage

A

two phases:
1. Initial hypoxic injury
2. Reperfusion injury: Greatest damage occurs

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41
Q

SCC esophagus Risk factors

A

HPV, smoking, alcohol, poverty, caustic oesophageal injury, achalasia, tylosis, Plummer-Vinson syndrome, radiation, diets deficient in fruit/veg and frequent consumption of very hot beverages

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42
Q

Causes Pneumatosis Coli

A
  • Cystic Fibrosis, Asthma
  • COPD
  • IBD*
  • Steroids and Chemo
  • Scleroderma (and other connective tissue disease)
  • Gas producing bacteria e.g. clostridium
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43
Q

Is Pseudomembranous colitis specific to C-diff ?

A

Pseudomembranes are not specific and can be seen in ischaemic bowel and necrotising infections.

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44
Q

Appendiceal carcinoid clinical presentation ?

A
  • Usually asymptomatic and discovered incidentally at surgery*
  • Otherwise may present with appendicitis or mucocele (less common) due to obstruction
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45
Q

Appendiceal carcinoid benign or malignant ?

A
  • Almost always benign and distant spread is exceptionally rare*
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46
Q

Mucocele cause

A
  • Mucocoele = macroscopic appearance of the appendix when it is distended with mucus.

Cause
- benign or malignant chronic obstruction of the appendix such as mucosal hyperplasia, adjacent caecal tumor, mucinous cystadenoma/adenocarcinoma

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47
Q

Mucocele ruptures often, T or F ?

A

F, rarely ruptures

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48
Q

Celiac disease bowel changes

A
  • Dilated jejunum with complete loss of folds
  • Jejunum loses folds and look like normal ileum (reversal)
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49
Q

Whipples disease involvement site

A

Proximal jejunum

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50
Q

Whipple’s ddx ? (pseudo-whipples)

A

MAI (instead of T.Whipplei)
- distinction done with acid fast stain

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51
Q

Spigelian Hernia location

A
  • At the lateral border o f the rectus (Semilunar line)
52
Q

Richter Hernia

A

Contains only one wall of bowel and therefore does not obstruct.

These are actually at higher risk for strangulation.

53
Q

Femoral hernia location

A
  • Inferior to inferior epigastric
  • Medial to common femoral vein
  • Below the pubic tubercle* (both inguinal hernias above)
  • Obstruction more common than others*
54
Q

Which side of paraduodenal hernia more common ?

A

Left

55
Q

Features of left vs right paraduodenal hernia

A

Left (fossa of Lanzert)
- behind IMV

Right (fossa of Waldeyer)
- associated with Malrotation
- behind SMA and below duodenum

56
Q

Sigmoid vs Caecal volvulus features

A

Sigmoid
- Haustra lost
- Points RUQ

Caecal volvulus
- Haustra maintained
- Dilated small bowel loops

57
Q

Neuroblastoma good prognostic factors

A

o Age at diagnosis < 18 months
o Stage 4S/MS
o Localized tumor not involving vital structures
o Absent MYCN (N-myc) oncogene amplification

58
Q

Giant Hemangioma features and complication

A

Features:
- Incomplete fill in
- Peripheral calcifications
- Hemorrhage, Necrosis

Complications:
- Kasabach-Merritt syndrome: consumptive coagulopathy due to thrombocytopenia

  • Rupture with hemoperitoneum
59
Q

FNH test to do ?

A

Sulfur colloid hot

60
Q

OCP affect on FNH ?

A
  • OCP use has a trophic effect, but does not cause FNH**
61
Q

FNH association

A
  • Hemangiomas
  • Hepatic adenomas
  • Meningioma, Astrocytoma
  • AVMs
62
Q

4 Cirrhosis microscopic changes ?

A
  1. Bridging fibrous septae
  2. Regenerative nodules
  3. Architectural disruption
  4. Vascular derangement
63
Q

Hepatic adenoma 3 types

A

Inflammatory
- most common
- risk to bleed if >5cm
- associated with NAFLD, obesity, OCP
- small definite risk of cancer
- dystrophic vessels “telangiectatic”

HNF-1a
- ONLY in women
- associated with OCP
- Fat containing
- Multiple masses

B-catenin
- Cancer risk
- associated with Anabolic steroids, Glycogen storage disease, FAP
- MEN and WOMEN

64
Q

Hepatic adenoma Microscopic finding

A
  • Absence of portal and central vein and bile ducts**
  • Contains fat mainly in HNF-1a
65
Q

Management and prognosis of Hepatic adenoma (eg. b-catenin type)

A
  • B-catenin type resected even if asymptomatic
  • Tumors may regress on withdrawal of OCPs
  • Risk of rupture is increased in pregnancy**
66
Q

Serum AFP sensitivity for HCC screening

A
  • Serum AFP is elevated in 50% of patients with advanced HCC
  • Insensitive as a screening test as can be normal in patients with premalignant or early HCC.
67
Q

HCC major and other risk factors ?

A

Major
- HBV, HCV, alcohol, NASH

Others:
- Hereditary haemochromatosis, alpha-1 antitrypsin deficiency, Wilson disease, tyrosinaemia, glycogen storage disorders, Primary biliary cholangitis/cirrhosis, Hepatic adenoma

68
Q

PBC pathology and imaging and complication

A

Path:
- Destruction of small intrahepatic bile ducts, portal inflammation, and progressive scarring
- High AMA

Imaging:
- Lace-like fibrosis and periportal halo sign are seen together the sensitivity for primary biliary cholangitis can approach 70%
- Regional lymphadenopathy: tends to dominate in the gastrohepatic ligament and porta hepatis

Complication
- Cirrhosis

69
Q

HCC genetic changes

A

Early changes
- Activation of b-catenin
- Inactivation of p53

Precursors
- dysplastic nodule
- small cell change
- large cell change

70
Q

Hepatic adenoma associations/RFs

A
  • Diabetes**
  • Metabolic syndrome*
  • Obesity
  • Glycogen storage disease
  • Anabolic steroids
  • OCPs
71
Q

HBV transmission route in high vs low prevalence areas

A

High prevalence
- Transmission during childbirth accounts for 90% of HBV cases in high prevalence areas

Low prevalence
- Unprotected sex and IVDU are the chief modes of spread

72
Q

Aetiologies of Hepatitis

A
  • Viral hepatitides
  • Parasites
  • Drug induced (Paracetamol, ETOH)
  • Autoimmune
  • Steatohepatitis
  • Metabolic disease
73
Q

Hepatitis B
- how many % ends in chronic infection ?
- how many % makes full recovery and clearance ?
- How many % get acute fulminant hepatitis ?

A
  • 10% get chronic infection (c.f. HCV 90% chronic infection and 20% develops cirrhosis)
  • 90% make full recovery and clearance
  • 1% get acute fulminant hepatitis (HCV also very rare)
74
Q

Hepatitis B dsDNA or RNA ?

A
  • Partially dsDNA (c.f. HCV ssRNA)
75
Q

Hepatitis C association ?

A
  • Associated with Metabolic syndrome
  • Will give rise to insulin resistance and NAFLD
76
Q

Majority or Minority of HCV will clear virus ?

A
  • only Minority will clear virus* (c.f. Hep B Majority)
77
Q

Which hepatitis dependent on HBV ?

A

Hep D dependent on HBV either as co-infection or superinfection*

78
Q

Hepatitis E high mortality rate in what demographic ?

A
  • High mortality rate in pregnant women*
79
Q

Pancreatic serous cystadenoma
- Location
- Benign or malignant

A

Location
- Pancreatic head (most common)

Path
- Lots of small cysts , tend to be < 10mm separated by fibrous septa radiating from a central scar which may be calcified
- Benign

80
Q

Mucinous cystadenomas
- how many % associated with invasive component ?

A

Can be precursors to invasive pancreatic carcinoma, around 20% associated with invasive component –> need to be resected

81
Q

What pancreatic lesion is Peutz-Jegher associated with

A
  • IPMN
  • Pancreatic ductal adenocarcinoma
82
Q

Classic feature of Pancreatic insulinoma

A
  • Amyloid deposition**
83
Q

Features of Glucagonoma

A
  • Diabetes and skin rash
  • sometimes DVT and PE
84
Q

Features of VIPoma

A
  • Diarrhea
  • Hypokalemia
  • Achlorydia
85
Q

Features of Somatostatinoma

A
  • Diabetes
  • Biliary dyskinesia with stones
  • Steatorrhea
86
Q

Clinical findings of PBC including labs

A

Usually identified on work up of raised ALP and GGT when it is asymptomatic.

When symptomatic, there are insidious findings of fatigue and pruritus.

87
Q

What’s unique about PBC cirrhosis ?

A
  • Hepatomegaly cirrhosis (rather than shrunken)
  • Not all end stage PBC end up with cirrhosis
88
Q

What microscopic lesion is diagnostic of PBC ?

A
  • Florid duct lesion: small bile ducts are actively destroyed by lymphoplasmacytic inflammation with or without the formation of granulomas.
89
Q

Lab findings of PBC

A
  • characteristic laboratory finding is antimitochondrial antibodies. ALP and GGT are raised.
90
Q

What type of virus is HIV ?

A
  • Retrovirus
91
Q

Echinoccoccus granulosus vs Echinococcus multilocularis

A

Echinoccoccus granulosus (more common)
- dogs definitive host
- sheeps intermediate host
- human accidental host
- better prognosis*

Echinococcus multilocularis
- fox definitive host
- rodent intermediate host
- worse prognosis*

92
Q

Which layer of Hydatid cyst gives rise to daughter cyst

A
  • Endocyst layer
93
Q

Type I Hypersensitivity reaction
- type ?
- examples ?

A

Type I Hypersensitivity reaction
- Immediate
- IgE and Mast cell mediated

Examples
- Anaphylaxis
- Bronchial asthma
- Allergic rhinitis
- Food allergies

94
Q

Type II Hypersensitivity reaction
- type ?
- examples ?

A

Type II Hypersensitivity reaction
- Antibody mediated*
- IgG or IgM tags cell for phagocytosis

Examples
- Autoimmune haemolytic anaemia
- Pemphigus
- ANCA vasculitis
- Goodpasture
- Acute rheumatic fever
- Graves, myasthenia
- Pernicious anaemia

95
Q

Type III Hypersensitivity reaction
- type ?
- examples ?

A

Type III Hypersensitivity reaction
- Immune complex mediated
- Inflammation and tissue injury from immune complex deposition

Examples
- SLE
- Post strep GN
- PAN
- Serum sickness
- Reactive arhtirits

96
Q

Type IV Hypersensitivity reaction

A

Type IV Hypersensitivity reaction
- T-cell mediated
- Caused by inflammation resulting from cytokines produced by CD4 T cells, and cell killing by CD8 T cells

Examples
- Rheumatoid arthritis
- MS
- T1 DM
- IBD
- Psoriasis
- Contact sensitivity
- Tuberculin reaction

97
Q

CYSTICERCOSIS and NEUROCYSTICERCOSIS
- Human Definitive host vs intermediate host pathophysio

A

Human Definitive host
- by eating raw pork
- mature tapeworm in intestine without invasion
- mild Abdominal symptoms only

Human intermediate host
- by eating faecal materials of infected human
- eggs penetrates intestine then spreads everywhere
- leads to Neurocysticercosis (seizures)
- can also become intermediate host by eating their own poo*

98
Q

Stages of Cysticercosis/neurocysticercosis

A
  1. Larval tissue invasion
  2. Vesicular
  3. Colloidal vesicular
  4. Granular nodular
  5. Calcified
99
Q

Who gets a Nutmeg liver ?

A

Nutmeg liver: Inhomogeneous mottled appearance
- Budd Chiari
- Hepatic veno-occlusive disease
- Right heart failure
- Constrictive pericarditis

100
Q

Who gets massive caudate lobe hypertrophy ?

A
  • Budd-Chiari (chronic phase, caudate hypertrophy and peripheral atrophy)
  • Primary Sclerosing Cholangitis
  • Primary Biliary Cirrhosis
101
Q

Is portal HTN a contraindication to Liver transplant ?

A
  • NO, only makes it more challenging
102
Q

Normal transplant liver US features

A
  • Rapid systolic upstroke
  • RI between 0.5 - 0.7
  • Hepatic artery peak velocity <200cm/s
  • Hepatic artery is KING in a transplanted liver, it is the primary source of blood flow for the bile ducts
103
Q

PSC vs AIDS Cholangitis

A

AIDS Cholangitis
- Infection of the biliary epithelium {classically Cryptosporidium)
- Appearance mimics PSC with intrahepatic and/or extrahepatic multifocal strictures.
- The classic association/finding is papillarv stenosis (which occurs 60% of the time).

104
Q

Oriental Cholangitis (Recurrent pyogenic cholangitis) Features and Association ?

A
  • Dilated ducts that are full of pigmented stones
  • “Straight rigid intrahepatic ducts”
  • The anatomically longer, flatter left biliary system tends to make the disease burden left dominant
    (the opposite of hematogenous processes
    which favor the right lobe).

Association
- Clonorchiasis, ascariasis, and nutritional deficiency.

105
Q

Causes o f Portal Vein Pulsatility:

A

Right-sided CHF, Tricuspid Regurg, Cirrhosis with Vascular AP shunting.

106
Q

Causes o f Portal Vein Reversed Flow:

A

The big one is Portal HTN (any cause).

107
Q

Amyloidosis stains

A

Congo red stain – under ordinary light imparts a pink/red colour to tissue deposits

Apple-green birefringence of the stained amyloid when observed by polarised light microscopy

108
Q

Which type of amyloidosis worst prognosis and which one good

A
  • Prognosis very poor for AL type (<2 year survival).
  • Secondary amyloidosis AA type prognosis is better (Chronic inflammation, RA, TB, RCC etc)
109
Q

Cholesterol gallstone RF ?

A

female sex

middle age

obesity

positive family history

recent rapid weight loss**

110
Q

Sickle cell and Crohn disease cause what type of gallstone ?

A

Black Pigmented stone

111
Q

Acute vs Chronic hepatitis morphology ?

A

Periportal inflammation only seen in Chronic*

112
Q

Down Syndrome, which is not a feature

Alzheimer’s disease
Atlantoaxial subluxation
Leukaemia (500x risk of AML, 20x risk of ALL)
Duodenal atresia
Secondary biliary cirrhosis

A

Secondary biliary cirrhosis

113
Q

Cholangiocarcinoma risk factors ?

A
  • BRCA2
  • Opisthorchis spp. and Clonorchis spp.
  • PSC, PSC, hepatolithiasis, Caroli disease, choledochal cysts
114
Q

Wilson’s disease lab findings ?

A
  • FREE serum copper: Increased (*serum copper reduced)
  • Urinary copper: Increased

(everything else, including ceruloplasmin are reduced)

115
Q

Wilson’s disease manifestations ?

A

Hepatic
- Acute hepatitis
- Chronic hepatitis
- Cirrhosis
- Fulminant hepatic necrosis

Brain
- Abnormal T2 hyperintensity in the putamina is the most common MRI abnormality, followed by midbrain, pons, and thalamus
- dysarthria, dystonia, tremor, parkinsonism, choreoathetosis, and ataxia and gait anomalies

MSK
- premature osteoarthritis
- osteopenia

116
Q

NEC RF

A
  • Prematurity
  • Enteral feeding
  • Formula feeding (6x more common than breast feed)
  • First affects the terminal ileum and caecum
117
Q

List out Calcium, PTH, and phosphate levels for the 3 types of Hyperparathyroidism

A

Primary hyperparathyroid - high Ca, low phosphate, high PTH

Secondary hyperparathyroid - TRUE, low Ca, high PTH, and high phosphate

Tertiary hyperparathyroid - high Ca, and VERY high PTH, low phosphate

118
Q

Features may indicate that a polyp is higher risk

A

> 2cm

> 3 adenomas

high grade dysplasia

Villous features

119
Q

What are secondary causes of hemochromatosis ?

A
  • Iron transfusion
  • Thalassemia, Sickle cell
  • Bantu siderosis
120
Q

Differentials for Hemochromatosis

A

Amiodarone Therapy
- Iodine-containing antiarrhythmic medication
- Diffuse, homogeneously dense liver on NECT

Glycogen Storage Disease
- ↑ or ↓ attenuation of liver on NECT
- Depends on specific type of disease
- Associated with multiple hepatic adenomas (60%)

121
Q

Other signs of Hemochromatosis apart from liver

A
  • Dilated cardiomyopathy
  • Hepatomegaly: 90%
  • Arthralgia: 50%
  • Diabetes: 30%
  • Dilated cardiomyopathy
122
Q

GIST associated syndromes

A
  • Carneys triad
  • Carneys Stratakis syndrome
  • NF-1
123
Q

GIST
- arise from what cell ?
- stains what ?
- genetic mutation of what ?

A
  • Arise from interstitial cell of Cajal
  • CD117 (c-KIT) positive stain
  • SDH subunit gene alternation
124
Q

What is Medullary spong kidney disease

A

sporadic condition where the medullary and papillary portions of the collecting ducts are dysplastic and dilated and in most cases develop medullary nephrocalcinosis.

125
Q

What are the associated syndromes of GIST ?

A

Carneys triad
- Extra-adrenal Paraganglioma
- GIST
- Pulmonary Chondroma

Carneys stratikis

NF-1

126
Q
A

PATH FINAL (10 decks)

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