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General study MD3 > Abdominal > Flashcards

Abdominal Flashcards

1
Q

Definition of Gastro-esophageal reflux disease (GERD)

A

Condition in which stomach contents flow back into the esophagus, causing irritation to the mucosa. Reflux is primarily caused by an inappropriate, transient relaxation of the lower esophageal sphincter.

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2
Q

Gastro-esophageal reflux disease (GERD) presentation, investigations and treatment

A

Presn: retrosternal burning pain (heartburn) and regurgitation, presentation is variable and may also include chest pain and dysphagia.
Ix: esophagogastoduodenoscopy and/or 24hr pH test.
Rx: PPIs (e.g. pantoprazole), lifestyle modifications, medication, in some cases surgery.

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3
Q

GERD complications

A

Complications: esophagitis and chronic mucosal damage can cause barretts esophagus, a premalignant condition that can progress to adenocarcinoma.

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4
Q

Peptic ulcer disease etiology

A

Presence of one or more ulcerative lesions in the stomach or duodenum. Etiologies include infection with H pylori (most common), prolonged NSAID use, condition associated with overproduction of stomach acid (hypersecretory states) and stress.

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5
Q

Peptic ulcer disease treatment

A

Rx: Symptom control (e.g. acid lowering medication - antacids), H pylori eradication therapy (clarithromycin + amoxicillin + PPI) and withdrawal of causative agents. Antisecretory drugs (eg PPIs) which reduce stomach acid production, are continued for 4-8 weeks after eradication therapy and may be considered for maintenance therapy.

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6
Q

Coeliac disease pathophysiology

A

Maladaptive immune response to gluten, a protein found in many grains.
Often occurs in patients with other autoimmune illnesses, associated with HLA variants.
Gluten intolerance triggers an autoimmune reaction and production of autoantibodies that target tissue transglutaminase, specifically within the proximal small intestine.

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7
Q

Coeliac disease presentation, investigations, treatment

A

Presn: change in bowel habits and symptoms assoc w malabsorption (e.g. fatigue, weight loss, vitamin deficiency).
Ix: diagnostic tests include the detection of various antibodies, to confirm the diagnosis, an endoscopic biopsy from the small intestine is needed. Histopathological changes include villous atrophy and crypt hyperplasia.
Rx: Gluten free diet, if adhered to, increased risk of celiac-associated malignancies (e.g. intestinal lymphoma) is mitigated.

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8
Q

Hepatitis A transmission

A

Faecal-oral, endemic in tropical, subtropical regions

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9
Q

Hep A disease course and symptoms

A

Acute viral hepatitis, initial prodromal symptoms (fever and malaise) followed by jaundice. Self-limited, acute liver failure rarely occurs.
Prodromal symptoms resolve within 1-2 wks, jaundice can persist for 1-3 months.

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10
Q

Hep A diagnosis

A

Lab findings include high serum transaminase levels and mixed hyperbilirubinemia. Serological detection of anti-HAV IgM antibodies confirms diagnosis.

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11
Q

Hepatitis B transmission

A

Transmitted sexually, parenterally or vertically. After an intubation period of 1-6 months, most patients develop asymptomatic or mild inflammation of the liver, which resolves spontaneously within a few weeks to months. However, 5% of adult patients and 90% of infants infected perinatally develop chronic hep B.

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12
Q

Hepatitis B treatment

A

Supportive measures. For chronic active Hep B, nucleoside or nucleoside analogs (e.g. tenofovir) are the preferred agents for reducing viral replication and infectivity.

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13
Q

Hepatitis B Investigations

A

Serological testing initially includes measurement of Hep B surface antigen (HBsAg), hepatitis B surface antibody (anti-HBs) and hepatitis B core antibody (anti-HBc). A detectable serum anti-HBs (indicating seroconversion) is a sign of recovery or successful immunization.

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14
Q

Hepatitis C transmission

A

A bloodborne pathogen commonly transmitted through needlestick injuries in health care settings or through shared injection needles.

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15
Q

Hepatitis C disease course and presentation

A

Attacks liver cells and causes liver inflammation.
2wk to 6month incubation period. Malaise, fever, myalgias, arthralgias, RUQ pain, tender hepatomegaly, nausea, vomiting, diarrhea, jaundice, pruritus.
Screening plays a role in detecting HCV infection because most infected individuals are asymptomatic or mildly symptomatic.
Approx 85% of individuals with an acute infection that is not recognised and treated will develop chronic Hep C, which is associated with cirrhosis, hepatocellular carcinoma and increased mortality. Mixed cryoglobulinemia, lymphoma (esp B cell non-Hodgkin lymphoma), membranoproliferative glomerulonephritis + many more

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16
Q

Hepatitis C investigations

A

Presence of HCV antibodies and HCV RNA confirm the diagnosis. HCV infection can be safely and effectively treated with direct acting antivirals which have cure rates of over 95%

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17
Q

Alcohol related fatty liver disease investigation results

A

AST>ALT (both elevated). Elevated GGT, elevated serum ferritin, macrocytic anemia, elevated CDT. US; mild hepatomegaly, blood vessels cannot be visualized, increased liver echogenicity because of steatosis. CT; decreased liver attenuation. Transaminase levels, imaging studies

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18
Q

Non-alcoholic fatty liver disease pathophysiology

A

Excess energy supply -> insulin resistance -> increased circulating dietary sugars and FFAs -> hepatic FFAs -> triglyceride synthesis -> hepatic steatosis. MASH cirrhosis; oxidative stress, ER stress and inflammasome activation -> inflammation and hepatocyte stress and/or death -> fibrogenesis -> cirrhosis

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19
Q

Non-alcoholic fatty liver disease investigation results

A

Normal or increased AST and/or ALT. AST/ALT ratio usually <1, AST/ALT ratio of >1 may indicate progression to cirrhosis. Normal or decreased serum albumin. CBC: normal or decreased platelet count

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20
Q

Non-alcoholic fatty liver disease definition

A

Accumulation of excess fat in hepatocytes in individuals with at least one cardiometabolic RG (e.g. HTN, impaired glucose tolerance) in the absence of an alternative cause (e.g. heavy alcohol uses, drug induced liver injury). MASH(NASH); chronic hepatocellular inflammation and damage.

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21
Q

Cirrhosis clinical findings (5)

A

Jaundice
Hepatosplenomegaly
Ascites
Skin changes (spider angiomata, palmar erythema, caput medusae)
Hormonal changes (gynecomastia, hypogonadism, sexual dysfunction)
Abdominal distension.

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22
Q

Hepatocyte damage investigation findings (2)

A

Elevated liver enzymes
Hyperbilirubinemia

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23
Q

Impaired hepatic synthetic function investigation findings (2)

A

Prolonged prothrombin time
Low albumin

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24
Q

Cirrhosis diagnosis confirmation

A

Abdominal ultrasound - shrunken heterogenous liver parenchyma with a nodular surface.
Liver biopsy if results from other diagnostic modalities are inconclusive

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25
Q

Primary hepatocellular malignancy presentation

A

HCC usually asymptomatic in early stage, ascites, jaundice
Advanced HCC; abdominal pain, weight loss, anorexia

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26
Q

Most common malignant liver lesion

A

Metastatic liver disease

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27
Q

Typical primary tumor sites for metastatic liver disease (3)

A

GI tract (colon, stomach, pancreas)
Lung
Breast

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28
Q

Metastatic liver disease abdominal ultrasound findings

A

’Bullseye’ with a hyperechoic center and hypoechoic periphery.

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29
Q

Metastatic liver disease CT abdomen findings

A

Recommended imaging modality for suspected liver metastases, multiple hypodense lesions (rarely; solitary metastases)

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30
Q

Is viral or bacterial leading cause of infective gastroenteritis? and what are the most common pathogens? (4)

A

Viral - Norovirus, rotavirus, enteric adenovirus, CMV.

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31
Q

Infective gastroenteritis bacterial pathogens (7)

A

Campylobacter
Salmonella
Shigella
Yersinia
Vibrio cholerae
E coli
Clostridioides difficile

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32
Q

Infective gastroenteritis alarm symptoms & criteria (9)

A

Sepsis,
Intense abdominal pain
Severe dehydration
Electrolyte abnormalities
Age >65
Pregnancy
Weight loss
Bloody stool/rectal bleeding
Abnormal renal function.

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33
Q

Infective gastroenteritis investigations in severe or immunocompromised

A

Stool cultures followed by empiric Abx therapy may be considered

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34
Q

Crohn’s disease gene association

A

HLA-B27 association

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35
Q

Crohn’s disease basic pathophysiology

A

Unrestrained Th17 cell function leading to inflammation, tissue damage, obstruction, fibrotic scarring, stricture and strangulation of bowel

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36
Q

Ulcerative colitis definition

A

Inflammatory bowel disease characterised by chronic mucosal inflammation of the rectum, colon and cecum.
15-35yo and >55yo M=F.
HLA-B27 association.
Smoking ad appendectomy are protective factors.

37
Q

Ulcerative colitis location and disease spread

A

Ascending inflammation beginning in rectum and spreads continuously proximally. Inflammation limited to mucosa and submucosa.

38
Q

Ulcerative colitis common symptoms (4)

A

Bloody diarrhea
Abdominal pain
Tenesmus
Fecal urgency

39
Q

Ulcerative colitis treatment

A

5-aminosalicylic acids (e.g. mesalamine) are the mainstay of Rx for mild to moderate disease. Severe; corticosteroids or other immunosuppressants.
Proctocolectomy is curative and indicated in patients with complicated UC or dysplasia.

40
Q

Irritable bowel syndrome symptoms

A

Chronic abdominal pain - cramping sensation, periodic exacerbations, pain freq related to defacation, either relieved or worsened, altered bowel habits - diarrhea, constipation or mixed. Bloating, abdo distension and flatulence. Diarrhea - loose stools, small to mod volume, urgency after meals, sometimes tenesmus.

41
Q

IBS rome III criteria

A

(I) improvement after defacation, (II) onset of symptoms asssoc w bowel freq. (III) onset of symp. Assoc. w change in stool appearance

42
Q

IBS treatment

A

Low FODMAP diet, adequate fibre intake, Gentle laxatives (constipation pred.) vs loperamide (diorrhea pred.), Peppermint oil, hyoscine butylbromide (buscapan), mebeverine, Psychological therapies. Modification of gut microbiota

43
Q

Risk factors for GERD (4)

A

Obesity, stress, eating habits (e.g. heavy meals, lying down shortly after eating), changes in anatomy of the esophagogastric junction (e.g. hiatal hernia).

44
Q

What organism causes post-streptococcal glomerulonephritis

A

Group A beta-hemolytic streptococcus.

45
Q

Presentation of nephritic syndrome

A

Red-brown urine, proteinuria, edema, HTN, acute kidney injury (elevated serum creatinine)

46
Q

Causes of IgA nephropathy (berger disease)

A

Most common cause of primary (idiopathic) glomerulonephritis in resource-abundant settings.
Usually triggered by URTI or GIT infections.
Peak incidence in 20-30s M:F 2:1

47
Q

Definition of nephrotic syndrome

A

Heavy proteinuria (protein excretion greater than 3.5g/24hrs)
Hypoalbuminemia (less than 3.5g/dL)
Peripheral edema

48
Q

Pathophysiology of acute tubular necrosis

A

Prolonged and/or severe ischemia can lead to ATN (severe hypotension, hypovolemic shock - hemorrhage, severe dehydration, septic, cardiogenic or neurogenic shock, thromboembolism, thrombotic microangiopathy, cholesterol embolism, toxicity, sepsis, infections.

Results in histological changes, including necrosis, with denuding of the epithelium and occlusion of the tubular lumen by casts and cell debris.

49
Q

Definition of acute kidney injury

A

Sudden loss of renal function w subsequent rise in creatinine and blood urea nitrogen (BUN). Most frequently causes by decreased renal perfusion (prerenal) but may also be due to direct damage to the kidneys (intrarenal) or inadequate urine drainage (postrenal)

50
Q

Pre-renal causes of AKI

A

65% of all AKI
- Hypovolemia, haemorrhage, vomiting, diarrhea, sweating, burns, diuretics, poor oral intake, dehydration, hypercalcemia, hypotension, sepsis, cardiogenic shock, anaphylactic shock.
- Drugs: NSAIDs, ACEIs, cyclosporine, tacrolimus

51
Q

Intrarenal causes of AKI

A

35% of all AKI
- ATN, ischemia, nephrotoxic drugs, endogenous toxins, glomerulonephritis

52
Q

Postrenal causes of AKI

A

5% of all AKI
- Any condition that results in bilateral obstruction of urinary flow from renal pelvis to urethra, BPH, tumors (bladder, prostate, cervical, metastases, stones, clots, neurogenic bladder, posterior urethral valves)

53
Q

UTI causing agents

A

E Coli (most common)
Staph saphrophyticus
Klebsiella pneumoniae
Proteus mirabilis
Enterobacter species
Pseudomonas aeruginosa

54
Q

Risk factos for UTIs

A

Sexual intercourse, catheters, pregnancy, F>M,

55
Q

Clinical features of UTI (lower and upper)

A

Lower UTIs (bladder and urethra):
- Dysuria
- Suprapubic pain
- Urinary urgency
- Increased frequency
- Hematuria

Upper UTIs (kidneys and ureters)
- Fever
- Flank pain
- Renal angle tenderness
- Fatigue/malaise
- N+V

56
Q

Treatment for UTI

A

First line empiric Abx therapy for uncomplicated:
- Oral nitrofurantoin, trimethoprim/sulfamethoxazole or fosfomycin for up to 7 days

For complicated; broad spectrum Abx:
- Fluroquinolones, beta lactams; ceftiaxone, ampicillin/sublactam, for 7-14 days.

Abx prophylaxis for recurrent UTIs

57
Q

Pelvic examination indications for cystitis

A

If S&S suggesting vaginitis or urethritis are present

58
Q

Definition of pyelonephritis

A

Infection of renal pelvis and parenchyma, usually assoc w ascending bacterial infection of the bladder.

59
Q

Investigation findings for pyelonephritis

A

Urinalysis shows pyuria and bacteriuria, WBC cases, positive nitrites.

Urine cultures should be taken in all patients before initiating treatment to identify the pathogen and possible antibiotic resistance.

60
Q

Definition of cholecystitis

A

Acute inflammation of the gallbladder. Typically due to cystic duct obstruction by a gallstone (acute calculous cholecystitis)

61
Q

Clinical presentation of cholecystitis

A

RUQ pain postprandial
Positive murphys sign
Fever
Guarding
Malaise
N+V

62
Q

Investigations and findings for cholecystitis

A

Ultrasound - gallbladder distension, wall thickening, edema and pericholecystic fluid
Blood cultures
LFTs: signs of cholestasis (increased bilirubin, ALP, GGT) are uncommon in cholecystitis, may be mild elevations in AST and ALT
CBC: Increased CRP, leukocytosis

63
Q

Definition of acute cholangitis

A

Bacterial infection of the biliary tract, typically secondary to biliary obstruction and stasis (e.g. due to choledocholithiasis (presence of gallstones in common bile duct), biliary stricture)

64
Q

Presentation of acute cholangitis

A

Charcot triad (RUQ pain, fever and jaundice)

65
Q

Investigations and findings in acute cholangitis

A

LFTs: evidence of cholestasis (elevated bilirubin, GGT, ALP)
Systemic inflammation (elevated CRP, leukocytosis)

66
Q

Treatment for acute cholangitis

A

Urgent biliary drainage within 48 hours

67
Q

Causes of pancreatitis

A

Biliary gallstones (40%)
Alcohol use (20%)
Idiopathic (25%)
Hypercalcemia
Hypertriglyceridemia induced
Drug induced (steroids, loop and thiazide diuretics)
Scorpion stings
Trauma

68
Q

Clinical presentation of pancreatitis

A

Sudden, severe epigastric pain that radiates to back
N+V
Epigastric tenderness on palpation

69
Q

Investigations and findings for pancreatitis

A

CT abdomen
Elevation of serum lipase or amylase >3x ULN

70
Q

Causes of appendiceal obstruction

A

Fecaliths (hard fecal masses)
Calculi
Lymphoid hyperplasia
Infectious processes
Benign or malignant tumors

71
Q

Appendicitis clinical presentation

A

Pain RLQ (beginning peri-umbilical)
Loss of appetite
Fever
Mcburneys point tenderness
Anorexia
N+V
indigestion
Flatulence
Bowel irregularity
Diarrhoea
Malaise

72
Q

Appendicitis investigations and findings

A

CBC: mild leukocytosis (WBC count >10,000 cells/microL), elevated CRP
Elevate creatinine, electrolyte abnormalities
Urine serum B-hCG test performed in all women of reproductive age to rule out pregnancy, ectopic pregnancy.
US/CT abdomen

73
Q

Causes of diverticulitis

A

Combination of increased intraluminal pressure (e.g. due to chronic constipation) and age-related weakness of the intestinal wall.
More common in older adults.
May progress to abscess or perforation

74
Q

Diverticulitis clinical presentation

A

LLQ pain (sigmoid colon most commonly involved), low grade fever, palpable mass, change in bowel habits, urinary urgency and frequency increased, acute abdomen

75
Q

Preferred diagnostic modality for diverticulitis

A

CT abdomen with IV contrast preferred
FOBT +ve

76
Q

Definition small bowel obstruction

A

Obstruction at the level of the duodenum, jejunum or ileum

77
Q

Clinical presentation small bowel obstruction

A

N+V
Abdominal pain (colicky, abrupt onset)
Distension and constipation or obstipation
Bowel sounds are increased and high pitched in early stages and decreased or absent in later stages
Dehydration - third space volume loss, electrolyte abnormalities

78
Q

Imaging findings small bowel obstruction

A

Dilation >3cm proximal to obstruction, dilated loops are predominantly central
Collapsed bowel loops distal to obstruction
Multiple air-fluid levels (>2, diameter >2.5cm, different heights within same bowel loop)

79
Q

Lab findings suggestive of bowel ischemia

A

Metabolic acidosis with elevated serum lactate

80
Q

Causes of large bowel obstruction

A

Malignancy (colorectal carcinoma) most common cause
Diverticulits
Volvulus
Less common: strictures, adhesions, fecal impaction, foreign body

81
Q

Imaging findings large bowel obstruction

A

Dilation >6cm

82
Q

Most common types of osephageal cancer? Risk factors for each

A

Squamous cell carcinoma and adenocarcinoma account for over 95% of malignant tumors
ACC now most common

SCC RFs: smoking and alcohol
ACC RFs: Barretts esophagus with intestinal metaplasia (complication of GERD), obesity and smoking are risk factors for ACC

83
Q

Osephageal cancer clinical presenation

A

Progressive dysphagia and weight loss
Regurgitation of saliva or food uncontaminated by gastric secretions
Blood loss from esophageal and esophaogastric junction is common and may result in deficiency anemia

84
Q

How is oesophageal cancer diagnosed?

A

Histological examination of tumor tissue. A diagnostic biopsy may be obtained by upper endoscopy or, if metastases are present by image guided biopsy of metastatic site

85
Q

Risk factors for gastric cancer

A

Infection with H pylori major risk factor
GERD
High sodium diet
Tobacco use

86
Q

Most common type of gastric cancer

A

Adenocarcinoma (95%) - intestinal or diffuse

87
Q

Clinical presentation of gastric cancer

A

Most patients symptomatic, weight loss and persistent abdominal pain (epigastric, vague progressing to severe) are the most common symptoms at initial diagnosis.
Nausea or early satiety, gastric outlet obstruction from an advanced distal tumour.

88
Q

How do you confirm gastric cancer?

A

Confirmed with upper endoscopy and biopsy.

89
Q
A

General study MD3 (8 decks)

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