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General study MD3 > Abdominal > Flashcards

Abdominal Flashcards

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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
Primary hepatocellular malignancy presentation
HCC usually asymptomatic in early stage, ascites, jaundice Advanced HCC; abdominal pain, weight loss, anorexia
26
Most common malignant liver lesion
Metastatic liver disease
27
Typical primary tumor sites for metastatic liver disease (3)
GI tract (colon, stomach, pancreas) Lung Breast
28
Metastatic liver disease abdominal ultrasound findings
’Bullseye’ with a hyperechoic center and hypoechoic periphery.
29
Metastatic liver disease CT abdomen findings
Recommended imaging modality for suspected liver metastases, multiple hypodense lesions (rarely; solitary metastases)
30
Is viral or bacterial leading cause of infective gastroenteritis? and what are the most common pathogens? (4)
Viral - Norovirus, rotavirus, enteric adenovirus, CMV.
31
Infective gastroenteritis bacterial pathogens (7)
Campylobacter Salmonella Shigella Yersinia Vibrio cholerae E coli Clostridioides difficile
32
Infective gastroenteritis alarm symptoms & criteria (9)
Sepsis, Intense abdominal pain Severe dehydration Electrolyte abnormalities Age >65 Pregnancy Weight loss Bloody stool/rectal bleeding Abnormal renal function.
33
Infective gastroenteritis investigations in severe or immunocompromised
Stool cultures followed by empiric Abx therapy may be considered
34
Crohn's disease gene association
HLA-B27 association
35
Crohn's disease basic pathophysiology
Unrestrained Th17 cell function leading to inflammation, tissue damage, obstruction, fibrotic scarring, stricture and strangulation of bowel
36
Ulcerative colitis definition
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
Ulcerative colitis location and disease spread
Ascending inflammation beginning in rectum and spreads continuously proximally. Inflammation limited to mucosa and submucosa.
38
Ulcerative colitis common symptoms (4)
Bloody diarrhea Abdominal pain Tenesmus Fecal urgency
39
Ulcerative colitis treatment
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
Irritable bowel syndrome symptoms
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
IBS rome III criteria
(I) improvement after defacation, (II) onset of symptoms asssoc w bowel freq. (III) onset of symp. Assoc. w change in stool appearance
42
IBS treatment
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
Risk factors for GERD (4)
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
What organism causes post-streptococcal glomerulonephritis
Group A beta-hemolytic streptococcus.
45
Presentation of nephritic syndrome
Red-brown urine, proteinuria, edema, HTN, acute kidney injury (elevated serum creatinine)
46
Causes of IgA nephropathy (berger disease)
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
Definition of nephrotic syndrome
Heavy proteinuria (protein excretion greater than 3.5g/24hrs) Hypoalbuminemia (less than 3.5g/dL) Peripheral edema
48
Pathophysiology of acute tubular necrosis
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
Definition of acute kidney injury
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
Pre-renal causes of AKI
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
Intrarenal causes of AKI
35% of all AKI - ATN, ischemia, nephrotoxic drugs, endogenous toxins, glomerulonephritis
52
Postrenal causes of AKI
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
UTI causing agents
E Coli (most common) Staph saphrophyticus Klebsiella pneumoniae Proteus mirabilis Enterobacter species Pseudomonas aeruginosa
54
Risk factos for UTIs
Sexual intercourse, catheters, pregnancy, F>M,
55
Clinical features of UTI (lower and upper)
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
Treatment for UTI
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
Pelvic examination indications for cystitis
If S&S suggesting vaginitis or urethritis are present
58
Definition of pyelonephritis
Infection of renal pelvis and parenchyma, usually assoc w ascending bacterial infection of the bladder.
59
Investigation findings for pyelonephritis
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
Definition of cholecystitis
Acute inflammation of the gallbladder. Typically due to cystic duct obstruction by a gallstone (acute calculous cholecystitis)
61
Clinical presentation of cholecystitis
RUQ pain postprandial Positive murphys sign Fever Guarding Malaise N+V
62
Investigations and findings for cholecystitis
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
Definition of acute cholangitis
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
Presentation of acute cholangitis
Charcot triad (RUQ pain, fever and jaundice)
65
Investigations and findings in acute cholangitis
LFTs: evidence of cholestasis (elevated bilirubin, GGT, ALP) Systemic inflammation (elevated CRP, leukocytosis)
66
Treatment for acute cholangitis
Urgent biliary drainage within 48 hours
67
Causes of pancreatitis
Biliary gallstones (40%) Alcohol use (20%) Idiopathic (25%) Hypercalcemia Hypertriglyceridemia induced Drug induced (steroids, loop and thiazide diuretics) Scorpion stings Trauma
68
Clinical presentation of pancreatitis
Sudden, severe epigastric pain that radiates to back N+V Epigastric tenderness on palpation
69
Investigations and findings for pancreatitis
CT abdomen Elevation of serum lipase or amylase >3x ULN
70
Causes of appendiceal obstruction
Fecaliths (hard fecal masses) Calculi Lymphoid hyperplasia Infectious processes Benign or malignant tumors
71
Appendicitis clinical presentation
Pain RLQ (beginning peri-umbilical) Loss of appetite Fever Mcburneys point tenderness Anorexia N+V indigestion Flatulence Bowel irregularity Diarrhoea Malaise
72
Appendicitis investigations and findings
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
Causes of diverticulitis
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
Diverticulitis clinical presentation
LLQ pain (sigmoid colon most commonly involved), low grade fever, palpable mass, change in bowel habits, urinary urgency and frequency increased, acute abdomen
75
Preferred diagnostic modality for diverticulitis
CT abdomen with IV contrast preferred FOBT +ve
76
Definition small bowel obstruction
Obstruction at the level of the duodenum, jejunum or ileum
77
Clinical presentation small bowel obstruction
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
Imaging findings small bowel obstruction
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
Lab findings suggestive of bowel ischemia
Metabolic acidosis with elevated serum lactate
80
Causes of large bowel obstruction
Malignancy (colorectal carcinoma) most common cause Diverticulits Volvulus Less common: strictures, adhesions, fecal impaction, foreign body
81
Imaging findings large bowel obstruction
Dilation >6cm
82
Most common types of osephageal cancer? Risk factors for each
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
Osephageal cancer clinical presenation
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
How is oesophageal cancer diagnosed?
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
Risk factors for gastric cancer
Infection with H pylori major risk factor GERD High sodium diet Tobacco use
86
Most common type of gastric cancer
Adenocarcinoma (95%) - intestinal or diffuse
87
Clinical presentation of gastric cancer
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
How do you confirm gastric cancer?
Confirmed with upper endoscopy and biopsy.
89
Definition of primary sclerosing cholangitis
Progressive chronic inflammation of both the intrahepatic and extrahepatic bile ducts. - Strong association with ulcerative colitis - Etiology unknown - RUQ pain, pruritis, fatigue, weight loss.
90
Lab test results in primary sclerosing cholangitis
Findings of cholestasis: - Elevated alkaline phosphatase (ALP) - Elevated gamma-glutamyltransferase (GGT) - Normal or elevated conjugated bilirubin pANCA positive in 80%
91
Diagnostic test for primary sclerosing cholangitis
MRCP - magnetic resonance cholangiopancreatography or ERCP - endoscopic retrograde cholangiopancreatography
92
Treatment for primary sclerosing cholangitis
No medications prevent disease progression Liver transplantation is the only curative treatment
93
Definition of primary biliary cholangitis
A chronic progressive liver disease of autoimmune origin that is characterised by intralobular bile ducts - Pathogenesis unclear - Frequently associated with other autoimmune conditions and primarily affects middle aged women
94
Clinical features of primary biliary cholangitis
Typically asymptomatic - Fatigue most common initial symptom - In advanced disease, increased fibrotic changes lead to typical signs of cholestasis (e.g. jaundice), portal hypertension (e.g. ascites, gastrointestinal bleeding) and severe hypercholesterolemia (e.g. xanthomas, xanthelasmas)
95
Diagnostic findings and confirmatory tests for primary biliary cholangitis
Elevated alkaline phosphatase (ALP) Elevated Antimitochondrial antibodies (AMA) Liver biopsy
96
Treatment for primary biliary cholangitis
Supportive care, e.g.management of cholestasis-associated pruritus, and slowing disease progression with ursodeoxycholic acid. Liver transplantation is the only definitive treatment.
97
Hepatitis A transmission
Fecal-oral transmission
98
Hepatitis A clinical presentation
Recently returned traveller - tropical or subtropical Prodromal symptoms - fever, malaise Jaundice - may persist for 1-3 months
99
Lab findings hepatitis A
High serum transaminase levels and mixed hyperbilirubinemia
100
Treatment for hepatitis A
Supportive - typically self-limited
101
Hepatitis B - transmission, clinical features
Sexual, parenteral or vertical transmission Incubation period 1-6 months - Most patients develop asymptomatic or mild inflammation of the liver, which usually resolves within a few weeks to months - 5% of adult patients and 90% of children infected parenterally develop chronic hepatitis B - Individuals with chronic hepatitis B may be asymptomatic carriers or develop ongoing hepatic inflammation with increased risk of cirrhosis and hepatocellular carcinoma.
102
Hepatitis B serology results
Hepatitis B surface antigen (HBsAg) - first evidence of infection, presence for >6 months indicates a chronic infection - Anti-HBs is corresponding antibody, indicates immunity to HBV due to resolved infection or vaccination Hepatitis B core antigen (HBcAg) - Anti-HBc: Anti-HBc IgM indicates recent infection with HBV (within <6months) - Anti-HBc IgG: indicates resolved or chronic infection Hepatitis B e antigen (HBeAg) - indicates active viral replication and thus high transmissibility and a poor prognosis - Anti-Hbe: indicates long term clearance of HBV and thus low transmissibility
103
Hepatitis B treatment
Supportive care as needed Avoid hepatotoxic medications Avoid alcohol, encourage weight loss Liver transplantation in patients with end stage liver disease or emergency fulminant hepatic failure Antivirals for chronic hepatitis B: - Tenofovir disoproxil fumarate (TDF) or tenofovir alafenamide (TAF) (preferred) - Entecavir (preferred) - Pegylated interferon alfa (PEG-IFN-a)
104
Hepatitis C - transmission, clinical features
Bloodborne - needlestick injuries, needle sharing Screening needed as most individuals asymptomatic - Approx. 85% of individuals with acute infection that is not recognised and treated will develop chronic hepatitis C - Chronic hepatitis C associated with cirrhosis, hepatocellular carcinoma and increased mortality
105
Hepatitis C serology and diagnostics
Presence of Anti-HCV antibodies - EIA/ELISA immunoassay) and HCV RNA (qualitative PCR - if anti-HCV antibody test is positive) confirm the diagnosis Additional lab studies: - Elevated transaminases - Cholestasis parameters: elevated GGT, elevated alkaline phosphatase (ALP), elevated bilirubin - Liver synthetic function tests (alterations suggest cirrhosis): decreased albumin, decreased total protein, increased prothombin time/INR
106
Treatment of hepatitis C
The goal of treatment is sustained virologic response Refer patients with end stage liver disease for liver transplantation evaluation Antiviral therapy - always treated with a multidrug approach (no antivirals are approved as monotherapy) - Direct acting antivirals: target and inhibit HCV-encoded proteins that are essential for the HCV replication cycle Example regimens: Glecaprevir plus pibrentasvir Acute and chronic HCV treated with the same antiviral regimens Offer hepatis A and/or B vaccination to hepatitis A and B seronegative individuals
107
First line treatment regime for H pylori eradication
PPI (esomeprazole) + amoxicillin + clarithromycin twice daily for 7 to 14 days If hypersensitive to penicillins: replace amoxicillin with metronidazole
108

General study MD3 (16 decks)

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