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Internal Medicine > GIT > Flashcards

GIT Flashcards

1
Q

Name the test which dx the cause of Oropharyngeal dysphagia

A

Videofluoroscopic modified barium swallow

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2
Q

Name the test which dx oesophageal dysphagia

A

Manometry if motility issue

Barium swallow

Endoscopy with biopsy

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3
Q

What are the causes of oropharyngeal dysphagia?

A

stroke
advanced dementia,

oropharyngeal malignancy

or

neuromuscular disorder like myasthenia gravis

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4
Q

Important point of Achalasia

A

Sx for >5 yrs before receiving diagnosis and mild weight loss

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5
Q

How to t/m achalasia?

A

laparoscopic myotomy and pneumatic balloon dilation treatment of choice in pts with low risk of surgery.

Pts with high risk of surgery botulinum toxin injection, nitrates and calcium channel blockers (but exclude malignancy 1st)

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6
Q

Name the cause of pseudoachalasia

A

Due to oesophageal cancer not due to denervation

With Rapid symptom onset (<6mo),

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7
Q

What are the dx findings of diffuse oesophageal spasm?

A

Endoscopy—> usually normal

Esophagram—> corkscrew pattern

Manometry—>intermittent persistalsis with multiple simultaneous contractions

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8
Q

How to approach patient with GERD without alarming symptoms?

A

trial of daily PPI—>refractory—>change PPI or ↑ use of PPI twice daily—>persistent—->endoscopy or esophageal pH monitoring

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9
Q

How to approach GERD with Alarming symptoms?

A

Endoscopy before trial—>esophagitis due to autoimmune or Barrett’s esophagus—>treat accordingly—not esophagitis—>further evaluation (e.g manometry)

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10
Q

What are the alarming symptoms with GERD?

A

alarm symptoms (dysphagia, odynophagia, weight loss, anemia, GI bleeding, recurrent vomiting)

or men >50 with chronic (>5 years) symptoms or cancer risk factors (eg tobacco use)

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11
Q

How to d/f oesophageal strictures from oesophageal cancer?

A

Stricture has symmetrical circumferential narrowing on barium swallow

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12
Q

Triad of Globus sensation (HYSTERICUS)

A

sensation of a foreign body in the throat.

worse when swallowing saliva and is frequently associated with anxiety

Pain, dysphagia, dysphonia, or systemic symptoms are not typical for globus and suggest another condition

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13
Q

Name the medication which causes pill induced oesophagitis

A

Tetracycline
Potassium chloride/iron

Aldrendronate/Risedronate

Aspirin and NSAIDs

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14
Q

What are the endoscopy findings of Pill induced oesophagitis?

A

discrete ulcers with normal- appearing surrounding mucosa

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15
Q

Name the causes of oesophageal perforation

A

Oesophageal ulcer/pill/caustic/infectious

Instrumentation viz endoscopy

Spontaneous rupture such as Boerhaave syndrome

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16
Q

How oesophageal perforation presents?

A

Chest or abdominal pain with fever

Crunching sound on chest auscultation (Hamman sign)

Subcutaneous emphysema in the neck

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17
Q

What will be seen in CT scan and CXR of oesophageal perforation?

A

Wide mediastinum with pneumothorax

Air around para spinal muscles with pleural effusions

Pneumomediastinum

Oesophageal wall thickening with mediastinal air fluid level

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18
Q

Important point of oesophageal wall rupture

A

Water-soluble contrast is preferred (less inflammatory to tissues)—>non-diagnostic—>barium study (higher sensitivity)

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19
Q

What are findings in d/f tests of boerhaave syndrome?

A

Pleural fluid analysis::
Exudative with low pH and very high amylase

Chest X Ray::
Pneumomadiastinum and pleural effusion

CT OR Oesophagraphy with gastrograffin confirm the diagnosis

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20
Q

Endoscopic finding of Mallory Weiss year

A

Longitudinal laceration on endoscopy

Mucosal tear in stomach Or esophagus

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21
Q

Important point::

A

BUN ↑ in upper GI bleeding and not lower GI bleeding

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22
Q

Important point

A

H.pylori is important cause of adenocarcinoma and eradication is recommended before cancer removal to avoid future adenoCA development

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23
Q

What are the causes of Gastric outlet obstruction?

A

gastric malignancy

peptic ulcer disease

Crohn disease

strictures (with pyloric stenosis) 2* to caustic acid ingestion

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24
Q

Triad of Gastric Outlet Obstruction

A

Post prandial pain

Vomiting with early satiety

Positive ABDOMINAL SUCCUSSION SPLASH test

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25
Q

Important point of Celiac disease

A

If IgA serology is negative and suspicion is high—>measure total IgA or IgG based serologic testing should be done

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26
Q

Name the condition in which D-xylose test come true positive

A

proximal small intestinal mucosal disease—>most common celiac disease

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27
Q

Name the condition in which D-xylose test come false positive

A

delayed gastric emptying or impaired glomerular filtration.

Small intestinal bacterial overgrowth—>fermentation of d-xylose before absorption—course of antibiotic (rifamixin) will improve d-xylose absorption

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28
Q

Name the condition in which D-xylose test comes negative

A

normal in pancreatic enzyme deficiency

Crohn disease (due to involvement of distal small intestine)

lactose intolerance

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29
Q

Name the test which dx steatorrhea

A

Fecal fat tests (eg, Sudan stain on spot stool specimen or 72-hour collection) confirm steatorrhea

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30
Q

What are the biopsy findings of tropical sprue?

A

Small intestinal biopsy—>
blunting of villi,
infiltration of chronic inflammatory cells, including plasma cells, lymphocytes and eosinophils

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31
Q

Important point of lactose intolerance

A

There is no steatorrhea

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32
Q

What are the protective mechanism which prevent the growth of bacteria in intestine?

A

The proximal small intestine normally contains relatively minimal bacterial colonization due to gastric acidity and peristalsis.

Other protective mechanisms against SIBO include:::
- bacterial degradation by proteolytic digestive enzymes
- trapping of bacteria by intestinal mucus,
and
- an intact ileocecal valve preventing retrograde bacterial movement from the colon

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33
Q

Name the d/f test to dx Small intestine bacterial overgrowth

And
name the Abx to Rx the condition (ABx like Rifaximin or Neomycin )

A

1)Jejunum aspirate which show more than 10*5 organisms per mL
But this test is invasive

2) Carbohydrate breath test (either using glucose Or lactulose) which shows peak in breath hydrogen /methane (as CHO metabolise by bacteria
3) low B12 but high Folate as bacteria produce it

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34
Q

How SIBO occur?

A

All Conditions which alter small bowel motility result bacteria come from colon into small intestine result SIBO

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35
Q

What are the risk factors for zinc deficiency?

A

TPN formulations that lack zinc, IBD pts are at risk because of impaired absorption

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36
Q

Triad of Zinc Deficiency

A

alopecia with abnormal taste

bullous, with pustulous lesions surrounding body orifices and extremities

impaired wound healing.

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37
Q

What is the important feature of selenium deficiency?

A

Cardiomyopathy

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38
Q

Triad of COLLAGENOUS COLITIS

A

chronic watery diarrhea in which colon is frequently involved

colonoscopy shows normal mucosa.

Biopsy shows mucosal subepithelial collagen deposition

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39
Q

Important point of Irritable bowel syndrome

A

Following signs/symptoms suggest other disorder than IBS:::

Rectal bleeding
Worsening abdominal pain /nocturnal

Weight loss
Abnormal lab findings

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40
Q

What are the complications of ulcerative colitis?

A

Toxic mega colon
Primary sclerosing cholangitis

CRC
Erythema nodosum/ pyoderma gangrenosum

Spondyloarthritis

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41
Q

Important point for toxic megacolon

A

Opioids are Avoided due to antimotility effect that can promote perforation.

Discontinue other anti-motility drugs like loperamide and anticholinergic agents

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42
Q

Name the surgical method for Toxic mega colon

A

Emergency surgery (subtotal colectomy with end-ileostomy—treatment of choice) if colitis not resolved.

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43
Q

How to approach per rectum bleeding?

A
  • if age >50 yrs Or Red flags = colonoscopy
  • If age 40-49 w/o red flags = sigmoidoscopy / colonoscopy
  • if age less than <40 yrs w/o red flags —> anascopy—>haemorrhoids Or no source identified then choose 2nd methods
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44
Q

Triad of Factitious diarrhoea

A

Excessive use of laxative

Watery diarrhoea esp nocturnal

biopsy findings: dark brown discoloration of colon
with lymph nodes shining through as pale patches (melanosis coli)—esp. in those using/abusing anthraquinone containing laxatives

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45
Q

What is the alternative dx of factitious diarrhoea?

A

histological evidence of pigment in macrophages of lamina propria

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46
Q

Important feature of Diverticular diseases

A

Association with chronic constipation And bleeding is usually painless

Alcohol—>↑ diverticula formation but not ↑ risk of diverticular complications

Ct (oral & IV contrast) used for dx acute diverticulitis

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47
Q

Name the complications of Acute diverticulitis

A

Associated with

abscess,

perforation,

obstruction

or fistula formation

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48
Q

How to t/m abscess due to diverticulitis?

A

**Fluid collection <3 cm—> IV antibiotics and observation—>surgery for pts with worsening symptoms

**fluid collection >3cm—>CT-guided percutaneous drainage—>if Sx not controlled by 5th day—>surgical drainage and debridement

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49
Q

Important point for acute diverticulitis

A

Barium enema, sigmoidoscopy and colonoscopy—>Not done in acute diverticulitis.

Colonoscopy—>performed after resolution of acute diverticulitis to rule out CRC

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50
Q

What are the CT-findings of acute diverticulitis?

A

CT scan:

inflammation in pericolic fat, presence of diverticula,

bowel wall thickening,
soft tissue masses (eg phlegmons),

and pericolic fluid collection suggesting abscess (upright x-ray shows nonspecific findings

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51
Q

What are the causes of Colovesical Fistula?

A

Diverticular diseases (sigmoid MCC)

Crohn diseases

Malignancy viz colon/ bladder/ pelvic organs.

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52
Q

What are the clinical findings of Colovesical Fistula?

A

Air comes out at the end after passing urine

Stool in urine

Recurrent UTI due to mixed flora

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53
Q

What is the CT-scan finding of Colovesical Fistula?

A

Contrast in bladder with thicken colonic and bladder walls

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54
Q

Triad of acute mesenteric ischemia

A

Rapid onset of peri umbilical pain which is out of proportion

Per rectal fresh bleeding

Increase WBCs and amylase/phosphate

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55
Q

How to dx Acute mesenteric ischemia?

A

Ct scan preferred
MR angiography

If dx unclear then Mesenteric angiography

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56
Q

CT scan findings of Acute mesenteric ischemia

A

focal or segmental bowel wall thickening

pneumatosis intestinalis

small bowel dilation

mesenteric stranding and mesenteric thrombi

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57
Q

Important point of acute mesenteric ischemia

A

There must be underlying thrombotic condition to develop this disorder

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58
Q

How to t/m Acute mesenteric ischemia?

A

open embolectomy with vascular bypass or endovascular thrombolysis

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59
Q

Triad of chronic mesenteric ischemia

A

Atherosclerosis as a cause

Post prandial pain with food aversion result weight loss

Signs of malnutrition and abdominal bruit

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60
Q

How to dx Chronic mesenteric ischemia?

A

CT angiography (preferred)

Doppler U/S

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61
Q

At what site of abdomen “Ischemic colitis” is mc?

A

Splenic flexure

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62
Q

What are the findings in d/f imaging used to dx ISCHEMIC COLITIS?

A

CT scan—> Thickened bowel wall / double Halo sign / pneumatosis coli

Colonoscopy—> mucosal pallor Or cyanosis/ petechia / haemorrhage

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63
Q

Important point of RETROPERITONEAL HEMATOMA

A

pt on anticoagulation (normal or supratherapeutic INR) —> raise suspicion for retroperitoneal hematoma

CT findings—> isodense area in retroperitoneum

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64
Q

Name the causes/ risk factors increases the risk of Angiodysplasia

A

advanced renal disease and vW disease due to ↑ bleeding tendency

Aortic stenosis al ↑ risk due to acquired vWF deficiency (from disruption of vW multimers as they traverse the turbulent valve space induced by AS—has been reported to remit after valve replacement

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65
Q

Features of Hyperplastic Polyp

A

Most common non-neoplastic polyps in the colon.

Arise from hyperplastic mucosal proliferation.

No further work-up needed

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66
Q

Features Of Hemartomatous polyp

A

Include juvenile polyp::
(a non-malignant lesion, generally removed due to the risk of bleeding)

Peutz Jeghers polyp::
(generally non-malignant).

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67
Q

What is the MC type of polyp found in the colon?

A

Adenoma

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68
Q

What feature of polyp suggest the cancerous condition?

A

Sessile> stalked (pedunculated)

tubular2.5 cm in size

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69
Q

Important point Cancer family syndrome or (Lynch syndrome II)

A

Lynch syndrome II is distinctly associated with a high risk of extracolonic tumors, the most common of which is endometrial carcinoma, which develops in up to 43% of females in affected families.

Also associated with ovarian and skin cancers

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70
Q

When to do screening of CRC if there is positive family Hx of FAP?

A

Begin at age 10-12 yrs of age

Colonoscopy every year

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71
Q

When to do screening of CRC if there is positive family Hx of Lynch syndrome?

A

Begin at age 20-25

Colonoscopy every 1-2 yrs

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72
Q

When to do screening of CRC if there is positive Hx of IBD?

A

Begin 8 yrs post diagnosis
(12-15 yrs if disease only in left colon)

Colonoscopy with biopsy every 1-2 yrs

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73
Q

When to do screening of CRC if there is positive family hx of adenomatous polyp Or CRC?

A

Colonoscopy at age 40 yrs OR 10 years before the age of diagnosis in the relative

Repeat every 3-5 yrs

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74
Q

What to do if colonic dysplasia is diagnosed?

A

Colonic dysplasia—>↑ risk of adenocarcinoma—>prophylactic colectomy advised

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75
Q

What are the portal HTN sign in patient of Cirrhosis?

A

Oesophageal varices

Splenomegaly
Ascites

Caput Medusa
Haemorrhoids

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76
Q

What are the signs of Hyper estrinism in patient of cirrhosis?

A

Spider angiomata
Gynecomastia

Loss of pubic hair
Palmar Erythema

Testicular atrophy

77
Q

Important of point of NAFLD

A

Usually there is increase ALT>AST ratio

If AST>ALT ratio increases it suggests progression to advance fibrosis and cirrhosis

78
Q

What are the peritoneal causes of Ascites?

A

Malignancy (Ovarian / Pancreatic)

Infection (Tb / fungal)

79
Q

What are the extra peritoneal causes of Ascites?

A

A = alcoholic hepatitis / acute liver failure

B = Budd chiari syndrome 
C = Cirrhosis
H = hypo albuminemia / HF 
M = malnutrition

N = Nephrotic syndrome

80
Q

What are the causes of ascites If total protein is less than “2.5g/dl””?

(Low protein ascites)

A

Cirrhosis

Nephrotic syndrome

81
Q

What are the causes of ascites If total protein is more than “2.5g/dl””?

(High protein ascites)

A

CHF
Constrictive pericarditis

Peritoneal carcinomatosis
Tb

Budd chiari syndrome
Fungal infection

82
Q

What does it meant to be increase SAAG ratio?

A

Due to increased hydrostatic pressure within the blood vessels of the hepatic portal system, which in turn forces water into the peritoneal cavity but leaves proteins such as albumin within the vasculature.

83
Q

What are the causes of Ascites if SAAG more than 1.1 g/dl (It indicates portal HTN)?

3Cs

A

Cardiac Ascites

Cirrhosis

Budd Chiari syndrome

84
Q

What are the causes of ascites if SAAG ratio is less than 1.1 g/dl?

Absence of portal HTN

Remember TPN

A

Tb
Peritoneal carcinomatosis

Pancreatic associates
Nephrotic syndrome

85
Q

How to t/m ascites?

A

Start with sodium and water restriction

Add diuretic therapy viz spironolactone if needed

Add loop diuretic if spironolactone doesn’t respond

If both diuretic therapy fails then slowly tapping the fluid but keep monitoring renal function

86
Q

Important point of ascites

A

Aggressive diuresis (>1 L/day) —>not recommended b/c of risk of hepatorenal syndrome

87
Q

Triad of HEPATIC HYDROTHORAX

A

Pleural effusion due to ascites—>defect in diaphragm

Right sided more common

Best option for treatment: liver transplant but Primary treatment: thoracocentesis followed by diuresis and salt restriction—>no response—>TIPS—>TIPS contraindicated—->pleurodesis

88
Q

What is the prophylactic treatment of Esophageal varices?

A

1st line = non-selective β-blockers

2nd line = endoscopic variceal ligation in those with contraindication to β-blockers

89
Q

what is the t/m of Esophageal varices?

A

Endoscopic sclerotherapy

Octreotide- long-acting somatostatin analog

90
Q

How to approach Esophageal varices?

A
  • Stabilze the patient with IV Fluids / Abx / Octreotide or Terlipressin

Then do urgent endoscopic therapy either sclerotherapy Or band ligation

91
Q

What to do even if ““bleeding stop”” after doing urgent endoscopic therapy for Esophageal varices?

A

Initiate Secondary prophylaxis such as BB plus endoscopic band ligation 1-2 weeks later

92
Q

What to do even if ““continued bleeding”” after doing urgent endoscopic therapy for Esophageal varices?

A

Balloon tamponade (temporary)–> Tips Or shunt surgery

93
Q

What to do even if ““Early Rebleeding”” after doing urgent endoscopic therapy for Esophageal varices?

A

Repeat Endoscopic therapy———->Hemorrhage–>TIPS Or Shunt Surgery

94
Q

Triad of Acute liver failure

A

Increase ALT/AST >1000U/L

Signs of hepatic encephalopathy

INR>1.5

95
Q

What is the most important prognostic factor of Acute liver failure?

A

PT

96
Q

Triad of ISCHEMIC HEPATOPATHY

A

Rapid and massive in AST and ALT, with modest ↑ in alkaline phosphatase.

Increase total bilirubin

Pts who survive underlying cause (eg septic shock or HF)–> LFTs return to normal within 1-2 wks.

97
Q

Name the dose dependent drug induced HEPATITIS

A

carbon tetrachloride

acetaminophen

tetracycline

and substances found in the Amanita phalloides mushroom.

98
Q

Name the dose independent drug induced HEPATITIS

A

isoniazid

chlorpromazine
halothane

and antiretroviral therapy.

99
Q

Name the drug which cause fatty liver

A

tetracycline

valproate

and anti-retrovirals

100
Q

Name the drug which cause Hepatitis

A

halothane

phenytoin

isoniazid

and alpha-methyldopa

101
Q

Name the drug which cause Cholestasis

A

chlorpromazine

nitrofurantoin

erythromycin

and anabolic steroids

102
Q

Name the drug which cause Toxic or fulminant liver failure

A

carbon tetrachloride and acetaminophen

103
Q

Important point

A

OCPs cause changes in LFTs without evidence of necrosis or fatty change

104
Q

Important point

A

While extrahepatic hypersensitivity manifestations like rash, arthralgias, fever, leukocytosis, and eosinophilia are common in patients with drug-induced liver injury

they are characteristically absent in cases of isoniazid-induced hepatic cell injury—Histologic picture is similar to viral hepatitis

105
Q

Important point

A

pts with AH have h/o chronic alcohol use (>7drinks/day or 100 g/day)—sometimes develop symptoms after acute ↑ in consumption.

In addition, alcoholic liver disease is unlikely with light to moderate alcohol intake (<15 drinks/wk for men, <10/wk for women).

A standard drink is equivalent to 12 oz of beer, 5 oz of wine, or 1.5 oz of 80-proof spirits (1 oz = 30 ml)

106
Q

How to managed Hepatic Encephalopathy?

A

Give Lactulose—-> If no response—-> rifaximin—-> Neomycin if patient Unable to take Rifaximin

Protein free diet

Keep hydrate the patient

Diuretics for ascites

107
Q

What are the diagnostic findings in lab test of SBP?

A

Paracentesis and PMN>250/mm3 are key diagnostic

Protein less than 1g/dl

SAAG >1.1g/dl

108
Q

How to t/m SBP?

A

Third Generation cephalosporins as empiric t/m

Quinolones for SBP prophylaxis

109
Q

Name the bacteria can cause SBP

A

E. coli&raquo_space; Klebsiella&raquo_space; Streph species

110
Q

Important point of cirrhosis

A

Pts with cirrhosis are normally hypothermic and >100 F warrants investigation

111
Q

What are the solid liver masses?

A

Focal nodular hyperplasia
Hepatic adenoma

Regenerative nodules

HCC
Liver mets

112
Q

What are the risk factors which increases the chances of hepatic adenoma formation?

A

Use of long term Contraceptives

Pregnancy

Anabolic steroid use

113
Q

How focal nodular hyperplasia occur?

A

Due to hyper-perfusion from anomalous arteries

Imaging will show arterial flow and central scar on imaging

114
Q

Name the solid liver masses which has high chance of hemorrhagic or malignant transformation

A

Hepatic adenoma

115
Q

What are the risk factors for hepatic angiosarcoma?

A

vinyl chloride

inorganic arsenic compounds

thorium dioxide

116
Q

Name the cause of direct jaundice in which ALT/AST/ALP is normal

A

Dublin Johnson syndrome

Rotor syndrome

117
Q

Name the cause of jaundice in which there is increase ALT/AST pre dominantly

A

HAT
H hemochromatosis
A autoimmune hepatitis /alcoholic
T toxin/drug induced

IV
Ischemic
Viral

118
Q

Name the cause of jaundice in which increase in ALP pre dominantly

A

PSC
PBC

Malignancy
Cholestasis of pregnancy

Choledocholithasis

119
Q

Triad of Gilbert syndrome

A

Decrease In enzyme activity with normal LFTs

Increase in indirect jaundice with underlying stressors

No apparent liver disease

120
Q

Triad of CN syndrome 1

A

Indirect jaundice with neurological impairment (Jaundice level >20 or up to 50)

Normal levels of enzymes in LFTs

Not affected by IV phenobarbital

121
Q

Triad of CN syndrome 2

A

Indirect jaundice with level <20

No neurological problem

IV phenobarbital level normalised bilirubin level

122
Q

What are the diagnostic test findings of Wilson disease?

A

old standard liver biopsy (copper >250mcg/gram dry weight),

confirmatory: ↓ ceruloplasmin level (<20 mg/dl)

↑ urinary copper excretion + Keyser Fleisher ring

123
Q

Name the test to be done if ALP and GGT both are increase plus US show dilated ducts

A

ERCP

124
Q

Name the test to be done if ALP and GGT both are increase plus US RUQ and AMA
ERCP both are normal

A

Consider liver biopsy / ERCP /observation

125
Q

Name the test to be done if ALP and GGT both are increase plus US show abnormal hepatic parenchyma OR positive AMA

A

Liver biopsy

126
Q

Triad of PBC

A

Direct jaundice SxS in female

+Ve AMA

autoimmune destruction of intrahepatic bile ducts

127
Q

How ursodeoxycholic acid (UDCA) cure the indirect jaundice?

A

UDCA is hydrophilic bile acid–> ↓ biliary injury by more hydrophobic endogenous bile acids—also ↑ biliary secretion and has anti-inflammatory and immunomodulatory effects–>delays histologic progression and improve sx and possibly survival

128
Q

What are the features of vanishing bile duct syndrome?

A

Progressive destruction of intrahepatic bile ducts

Histologic hallmark: ductopenia

129
Q

What are the causes of Ductopenia?

A

Most common cause of ductopenia: primary biliary cirrhosis.

Other causes:
failing liver transplantation, Hodgkin’s disease,

graft-versus-host disease, sarcoid, CMV infection,

HIV and medication toxicity

130
Q

Triad of PSC

A

Direct jaundice with Extra/Intra hepatic dilation or stricturing

Onion skin pattern on liver biopsy

ERCP or MRCP–> Beading

131
Q

What are the different mechanisms to develop Gallstones?

A

TPN Or Fasting:: no stimulus for CCK and gallbladder contraction–> gall bladder stasis

-Ileal resection Or Crohn’s disease so return of bile salt–>bile becomes supersaturated with cholesterol–>cholesterol gall stone formation due to ↑ concentration of bilirubin conjugates and total calcium in gall bladder

Estrogen–>↑ in cholesterol secretion Progesterone–> ↓ bile acid secretion and slows gallbladder emptying

132
Q

How to t/m Gallstones without symptoms?

A

No t/m necessary in most patients

133
Q

How to t/m Gallstones with typical biliary colic symptoms?

A

Elective laparoscopic cholecystectomy

Or Urodeoxycholic acid in pops surgical patients

134
Q

How to t/m complicated Gallstones?

A

Cholecystectomy within 72hrs

135
Q

What are the findings On CT scan of Gallstones ileus?

A

Gallbladder wall thickening

pneumobilia

and an obstructing stone

136
Q

How to t/m Gallstones ileus?

A

surgical removal of stone and either simultaneous or delayed cholecystectomy.

137
Q

Triad of Biliary colic

A

Pain occur when intake of meal and resolve within 4-6 hours

Due to obstructive cystic duct

No inflammatory SxS unlike cholecystitis

138
Q

Triad of Acute cholecystitis

A

RUQ pain when intake of meal and last longer than 6 hours

inflamed Gallbladder due to Obstructed cystic duct

Presence of SxS of inflammation unlike bilaru colic

139
Q

What is POSTCHOLECYSTECTOMY SYNDROME ?

A

PCS refers to persistent abdominal pain or dyspepsia (eg, nausea) that occurs either postoperatively (early) or months to years (late) after a cholecystectomy.

140
Q

How to t/m POSTCHOLECYSTECTOMY SYNDROME?

A

Treatment for PCS is directed at the causative factor:

ERCP with sphincterotomy is the treatment of choice for sphincter dysfunction

141
Q

What are the risk factors for the Acalculous cholecystits?

A

Prolonged Fasting Or TPN

Critical illness ( sepsis / ICU / On vent)

Severe trauma
Extensive burns

Recent surgery

142
Q

What are the image findings of acalculous cholecystits?

A

gallbladder wall thickening and distension and presence of pericholecystic fluid

143
Q

How to t/m acalculous cholecystits?

A

immediate antibiotics followed by percutaneous cholecystostomy under radiologic guidance.

Cholecystectomy with drainage of any associated abscesses—definitive treatment once pts condition improves

144
Q

Triad of EMPHYSEMATOUS CHOLECYSTITIS

A

Immunosuppression patients

Fever with RUQ pain and N/V

Air fluid level in gallbladder with gas in gallbladder wall which result in crepitus in abdominal wall adjacent to gallbladder

145
Q

Name the bacteria which cause EMPHYSEMATOUS CHOLECYSTITIS

A

Gas forming bacteria viz Clostridium and some strains of E.coli

146
Q

How to t/m EMPHYSEMATOUS CHOLECYSTITIS?

A

Emergent cholecystectomy with use of broad spectrum ABx

147
Q

What is Charcot triad in acute cholangitis?

A

Fever

RUQ pain

Jaundice

148
Q

What would be seen on imaging on acute cholangitis?

A

Biliary dilation on U/S Or CT scan

149
Q

How to t/m acute cholangitis?

A

ERCP with sphincterotomy

Or

Percutaneous trans hepatic cholangiography

With USE of Broad spectrum ABx

150
Q

What are the diagnostic findings of acute pancreatitis?

A

Epigastric pain radiates to back

Increase amylase/lipase >3 times normal limit

Imaging shows focal Or diffuse pancreatic enlargement with heterogeneous enhancement on CT. and if U/S diffusely enlarged and hypoechoic pancreas

151
Q

How to dx pancreatitis due to Gallstones?

A

RUQ U/S—> if non-Dx—>ERCP

HIDA Scan not use to dx pancreatitis rather used for cholecystits

152
Q

Important point of pancreatitis

A

If ALT increases think of biliary induced pancreatitis

153
Q

Important information of acute pancreatitis management

A

Pt should be NPO except essential medications like antiplatelet therapy in case of stent placement

Prophylactic antibiotics are not routinely used in acute pancreatitis—unless there is evidence of necrotizing pancreatitis with local infection

154
Q

Name the medication which causes acute pancreatitis

A

Valproate

Furosemide/thiazides

sulfasalazine, 5-ASA

azathioprine

didanosine, pentamidine

metronidazole, tetracycline

155
Q

What are the CT findings of drug induced Pancreatitis?

A

peripancreatic fluid and fat stranding

156
Q

Important point of chronic pancreatitis

A

Stool elastase—
marker for pancreatic exocrine function

low levels in CP rather than acute pancreatitis

157
Q

What does it meant by Severe Pancreatitis?

A

pancreatitis with involvement of at least one organ

158
Q

What are the CT findings of PANCREATIC PSEUDOCYST?

A

round, well circumscribed, encapsulated fluid collection

(usually no necrosis or solid material), thick fibrous capsule, containing enzyme-rich fluid, tissue and debris

159
Q

How to t/m pancreatic pseudocyst?

A

Minimal or no symptoms and without complications (eg pseudoaneurysm)—>expectant management (eg symptomatic therapy and NPO)—preferred initially 

Significant symptoms (abdominal pain, N/V), infected pseudocyst, evidence of pseudoaneurysm—>endoscopic drainage

160
Q

What are the inherited Rx factors for pancreatic cancer?

A

1st Degree relative with pancreatic cancer

Hereditary pancreatitis

Germline mutations (BRCA 1 and 2)(PJ syndrome)

161
Q

How to approach pancreatic head cancer?

A

U/S—> if non-Dx—>ERCP—>PTC

162
Q

Why U/S is not useful in pancreatic cancer at tail and body?

A

less visibility of tail and body due to overlying bowel gas and also less sensitive for detecting smaller tumors (<3cm)

163
Q

How to t/m hepatic adenoma?

A

If less than 5cm and asymptomatic–>stop COCP

If more than 5cm and symptomatic—> surgical resection

164
Q

How Hepatic hemangioma present on US?

A

NO CENTRAL SCAR

centripetal enhancement (from periphery to central

165
Q

Triad of Bile acid Diarrhea

A

Secretory diarrhea occur after removal of gallbladder

Persist even after fasting (unlike lactose intolerance)

Negative blood and stool work up

166
Q

How to manage bile acid Diarrhea?

A

Bile acid resins–>cholestyramine
colestipol
colesevelam

167
Q

What are the signs of hyper estrogen in Cirrhosis patient?

A

Spider angiomata
Breast formation

Palmar erythema
testicular atrophy

Loss of sexual hair

168
Q

What factors increases the chance of C.difficle infection?

A

1) Abx like Quinolone, Cephalosporins, clindamycin, pencillin

2) Decrease Gastric acid
3) Hospitalisation

4) Advanced age more than 65 yrs

169
Q

How to treat IBS?

A

Reassurance and Dietary modification

If constipation type—>fiber supplementation

If diarrhea—->Antidiarrheal like loperamide

170
Q

Lab presentation of alcohol

A

CBC shows increase WBC and neutrophilia

LFT shows increase AST ALT GGT
AST TO ALT ratio more than 2
AST and ALT increase upto 500

Also increase Ferritin

171
Q

How to treat IBD induced Toxic megacolon?

A

IV steroid like methylpred

Avoid invasive imaging like colonoscopy

172
Q

How Proctaglia fugax occur?

A

Due to spastic Contraction of anal sphincter
Or
Pudendal nerve compression

173
Q

Triad of Proctaglia fugax

A

recurrent rectal pain with pain free episodes

Unrelated to defecation

Normal physical Ex without lab abnormalities

174
Q

How to manage Proctaglia fugax?

A

Reassurance

Nitroglycerin ± biofeedback therapy for recurrent sxs

175
Q

Important point of IBS

A

SxS like rectal bleeding Or weight loss
Abnormal labs
Worsen abdominal pain esp at night

All above features of present—-> Exclude IBS as a dx

176
Q

How to approach dysphagia and odynophagia in patient with HIV?

Note point —> neither HSV nor CMV treat empirically

A

First check oral thrush
If present —>candida given fluconazole with no need of EGD

If no thrush or fail to respond empiric t/m
Then do EGD with biopsy

177
Q

Name the vaccine given in chronic liver disease

HABIT (B=P)

A

HA HAV / HBV
P pneumococcal
I flu
T Tdap

178
Q

Triad of Spontaneous bacterial peritonitis

A

High grade fever with abdominal tenderness

Low BP with Hypothermia

Paralytics ileus with severe infection

179
Q

How to dx and t/m SBP?

A

Dx test shows Neutrophils >250mm3

  • SAAG >1.1g/dl and total protein <1g/dl

Rx—> Quinolones (as ppx) and 3rd generation cephalosporin as Empiric

180
Q

Name the med for wilson disease treatment

A

1) Chelators like trientine or D pencillamine

2) zinc as it interfer absorption of copper.

181
Q

How PJ syndrome present?

A

Pigment macules on lips, buccal mucosa, palm / soles

Due to hemartomatous polyp result
Anemia due to polyp ruptured

Obstructive sxs or Intussusception
Rectal prolapse

182
Q

How to dx and manage Autosomal dominant PJ syndrome?

A

Dx —–> Genetic testing

Manage—-> annual anemia screening and cancer screening via Upper/lower EGD

183
Q

Red flags which need to be evaluated via colonoscopy

A

abdominal pain with change in bowel habit,

Wt loss, Iron deficiency anemia, Fx hx of colon cancer

184
Q

When to suspected Infected Pancreatic Necrosis and How to dx it?

A

Abdominal pain with signs of sepsis (after the onset of Acute necrotizing pancreatitis)

Dx:

  • CT abdomen shows Gas within the necrotic collection
  • Aspiration and culture of necrotic material
185
Q

How to tx Infected Pancreatic Necrosis?

A

IV ABx onced stabilize —>do Debridement

186
Q

What are the 4As of Hepatic encephalopathy?

A

Ataxia
Asterixis

Altered mental status
Altered sleep pattern

187
Q

What factors increases the risk of Hepatic encephalopathy?

H PRIDE

A

H hypovolemia
D drugs like sedatives narcotics

I infection like pneumonia UTI SBP
Increase Nitrogen load to GIT bleeding

P portosystematic shunting like TIPS
E lytes changes like low potassium

188
Q

Triad of Budd chiari syndrome

A

Ascities

Abdominal pain

HSM

189
Q

Name the condition leads to Budd chiari syndrome and how to dx?

A

Myeloproliferative disorder (PV)

Malignancy like HCC

OCP and pregnancy

Dx —>US Doppler abdominal (decrease hepatic vein flow)

Internal Medicine (14 decks)

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