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Bloc E - Final > Clinical > Flashcards

Clinical Flashcards

1
Q

Upper GI bleeding (UGIB) management?

A
  • Upper = up the ligament of Treizt
  • Major diagnosis: gastric or duodenal ulcer, gastric or oesophageal varices (due to portal hypertension from liver cirrhosis, high mortality rate), erosive esophagitis
  • After history and vital signs, we have to do lab tests (CBC, chemistry, liver and coagulation studies)
  • In upper GI bleeding, the blood urea nitrogen level typically increases to a greater extent than the creatinine level
  • Patients should undergo endoscopic evaluation within 12-24 hours
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2
Q

Lower GI bleeding (LGIB) management?

A
  • About 15 to 20% of patients who present with hematochezia (passage of red blood or clots per rectum), have an upper GI source of brisk bleeding
  • Same evaluation as UGIB
  • Most patients then need endoscopic evaluation
  • Flexible sigmoidoscopy/anoscopy, especially if anorectal/distal colon bleeding
  • Colonoscopy allows for diagnosis and possible hemostasis of amenable lesions
  • Red blood cell scan if major bleeding and the source cannot be identified by colonoscopy
  • Major causes: diverticulosis, internal hemorrhoids, ischemic colitis, ulcers
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3
Q

UGIB treatments?

A
  • ABCs (IV, intubation, INR correction)
  • Type and Cross-Match
  • Fluid resuscitation
  • Crystalloid
  • Blood
  • Risk stratification
  • Clinical
  • Endoscopic
  • Available treatments:
    • Injection
    • Thermal coagulation,
    • Mechanical compression (clips)
    • Hemostatic powders
    • Endoscopic therapy is reserved for lesions that have high-risk stigmata: we use proton pump inhibitors to suppress acid secretion and promote platelet aggregation
    • Alternative management for refractory bleeding: radiological percutaneous procedures, surgery and radiotherapy
    • Variceal UGIB treatment: pharmacotherapy + endoscopy + radiological therapy + temporarily balloon temponade/stenting
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4
Q

LGIB treatments?

A
  • Colonoscopy
  • Alternative therapies: angiographic embolization, surgery
  • Prognostic dependant on the source of bleeding
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5
Q

Obscure (middle) GIB?

A
  • Videocapsule endoscopy; enteroscopy
  • Most common in small intestine (not accessible by colonoscopy and endoscopy)
  • Vascular lesions are the most common cause, followed by iron deficiency
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6
Q

Dental carries Pathological factors?

A
  1. acid producing bacteria
  2. fermentable carbohydrates
  3. insufficient saliva (xerostomia)
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7
Q

Dental carries Protective factors?

A
  1. Fluoride
  2. Saliva flow
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8
Q

Main risk factor for dental carries?

A
  1. Poverty (social determinants of health)
  2. Lifestyle and behavioural
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9
Q

Caries disease process signs?

A
  1. Color: white, brown or back color
  2. Location: where biofilm can stagnate (root)
  3. Shape
  4. Tooth surface integrity
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10
Q

Stages of dental carries?

A

D1 – Subclinical initial lesion
D2 – Enamel non-cavitated lesions
D3 – Enamel cavitated lesions
D4 – Pulp lesions

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11
Q

Important prevention guidelines?

A
  • Children should not fall asleep with milk or juice
  • We should be aware of the sugar contained in the medication we prescribe
  • Brush the teeth and oral hygiene EARLY
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12
Q

Clinical manifestation of pancreas disease?

A

Pancreatitis

  • Sudden onset abdomen pain radiating to the back
  • May be relieved by leaning forward
  • +/- jaundice
  • Ecchymotic discoloration

Neoplastic (depends on location)

  • Head of the pancreas will likely block the ducts and the patient will present with symptoms earlier (jaundice, light stools, dark urine)
  • Body or tail usually present later when there is spreading to other organs (pain, weight loss).
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13
Q

Approach to liver problem?

A

1. History taking

Place of birth, family history, blood transfusion prior to 1990, alcohol, IV or nasal drugs, tattoos or piercing, vaccination/medical/dental care in other country, barber shops (razors), prison or military service, sex, metabolic syndrome

2. Liver function tests (LFTs)

Are NOT AST, ALT, ALP or GGT: these are karmers of liver injury NOT dysfunction

Function tests:

  1. PT, albumin, conjugated biliburin
  2. Glucose control, lipids
  3. Galactose elimination, caffeine clearance or aminopyrine breath test

The best liver function test: INR (vitamin K dependent clothing factor)

3. Ultrasound to determine if problem is intrahepatic or extrahepatic, blood flow, screen cancer

4. Fibroscan: stiffness of the liver, replaces biopsy

5. CT or MRI scans

6. Check for thyroid and celiac disease

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14
Q

Liver disease and decompensation?

A
  • Hepatitis B and C

HBSAG: hepatitis B surface is the most important serology test

Core anti-body: tells if you had a natural , not a vaccine

  • NASH
  • ETOH

Healthy –> fatty –> fibrosis –> cirrhosis

  • Drug induced liver injury
  • Autoimmune liver disease
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15
Q

Causes of cirrhosis?

A
  • Primary liver disorders: obesity
  • Bile ductal blockage
  • Drugs and toxins: alcohol
  • Infections: hepatitis B and C
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16
Q

Key pathologic feature of cirrhosis?

A

FIBROSIS

The key step in the pathophysiology of liver fibrogenesis is the balance between ECM deposition and removal. Histologically: kupffer cells reduced, endothelial cell, hepacotytes damage, lymphocytes and neutrophils ® created autocrine inflammation stimuli

LIVER FIBROSIS: THE SINGLE MOST IMPORTANT PREDICTOR OF MORTALITY

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17
Q

Cirrhosis diagnosis?

A
  1. Clinical features: obesity, hypertension, insulin resistance, fx, hepatomegaly…
  2. Biopsy: inflammation, FIBROSIS, cellular infiltration
  3. Imaging: IS, MRI, CT, transient Elastography (FibroScan)
  4. Biomarkers: APRI=[AST (/ULN) x 100] / Platelet (109/L) (value >2 means presence of cirrhosis), ALT, AST, biliburin, proinflammatory, cytokines…
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18
Q

Complications of cirrhosis?

A
  • Palmar erythema
  • Hypogonadism
  • Gynecomastia
  • Splenomegaly
  • Spider nevi, caput medusa (falciform ligament)
  • Ascites, edema: PH, hypoalbuminemia, 2nd hyperaldosteronism, arterial vasodilatation
  • Varices and hemorrhoids
  • Encephalopathy
  • Itching
  • Increased susceptibility to drug toxicity
  • Liver cancer
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19
Q

Treatment of cirrhosis?

A
  • Screening for HCC
  • Screening for endoscopic signs of portal hypertension
  • Transplantation MELD score > 15 (based on serum bilirubin and creatinine)
  • Treatment of complications: HE, ascites,
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20
Q

Risk factors of IBD?

A
  • Age – more likely among younger patients3
  • Ethnicity – more likely among Caucasians, in particular Ashkenazi Jews3
  • Family history – 15-25% risk of IBD if 1st degree relative affected. 60% concordance in monozygotic twins
  • Geography – more common in US and Europe4,5
  • Smoking – Active smokers are more than 2 times as likely to develop CD than nonsmokers, but less likely to develop UC3
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21
Q

Comparison UC and CD

A
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22
Q

Extraintestinal Manifestations of IBD?

A
  • C = Cholangitis (primary sclerosing cholangitis)
  • H = Hematologic (anemia, hemolysis, amyloid)
  • E = Eye (episcleritis, uveitis)
  • A = Arthritis (peripheral, axial)
  • T = Thromboembolism
  • S = Skin (e. nodosum, pyoderma gangrenosum)
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23
Q

What is celiac disease?

A
  • T cell mediated immune disease of the small intestine triggered by gliadin (gluten protein) found in wheat, barley and rye
  • Genetic factors (chromosome 6)
  • HLA DQ2 and DQ8 gene loci
  • > 98% in celiac disease but present in 30% of Caucasion’s: necessary but not sufficient
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24
Q

Diagnosis of celiac disease?

A

IgA EMA (endomysial antibodies)

–Gold standard.

–If treated, the test becomes negative.

IgA tTG (tissue transglutaminase)

–Cheaper and more available

–False-positive in patients with other auto-immune or liver diseases

–Decreases when on a gluten-free diet

–can be used to assess compliance (should fall to normal or “baseline” within 3-6 months)

–False negatives in IgA deficient patients (IgG TTG)

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25
Q

Clinical manifestations of celiac disease?

A
  • Mean age at presentation 45
  • Episodic diarrhea (up to 10x per day): nocturnal or early morning diarrhea is common
  • Distention
  • Steatorrhea
  • Flatulence
  • Weight loss
  • Vague abdominal discomfort/fatigue
  • Anemia: ion, folate, B12
  • Recurrent aphthous ulcers
  • Systemic manifestations: kidney disease, dermatitis herpetiformis, neuropsychoatric disease, metabolic bone disease
  • Complications: malignancy
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26
Q

Types of celiac disease?

A
  1. Classic or typical celiac disease: gluten-sensitive enteropathy found in association with villous atrophy, malabsorption (steatorrhea, wt loss, vit def) and resolution of symptoms and mucosal lesions on a gluten free diet
  2. Atypical celiac sprue: gluten-sensitive enteropathy with only minor GI symptoms, but atypical manifestations including anemia, osteoporosis, arthritis, neurological symptoms and infertility
  3. Asymptomatic (silent) celiac disease: gluten-sensitive enteropathy found after serologic screening in asymptomatic patients
  4. Latent (potential) celiac disease: Patients who have normal villous architecture on a gluten-containing diet (but have serological markers positive for celiac disease)
  5. Refractory celiac disease: Symptomatic, severe small intestinal villous atrophy but does not respond to at least 6 months of a strict gluten-free diet
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27
Q

Bile content?

A
  • The bile is an emulsion of bile salts (micelles), cholesterol and lecithin
  • Function is to absorb FAT
  • Bile gives poop its color. Absence of fecal bile salts makes stools white and is a sign of liver dysfunction. It is 95% reabsorbed and 5% excreted. Excess of bile secretion causes diarrhea.
28
Q

Regulation mechanisms of bile?

A
  • Secretin - stimulates FLOW by increasing Cl-rich fluid
  • Cholecystokinin (CCK) and gastrin stimulate bile generation and contraction of the gallbladder
  • Glucagon relaxes sphincter of Oddi
29
Q

Testing for bile problems?

A

Blood test of bilirubin: total, indirect and direct

30
Q

Risk factors for Cholelithiasis (gallstones)?

A
  • Genetics
  • Age
  • Obesity
  • Hyper-estrogenic states
  • Rapid weight loss
  • Bile stasis
31
Q

Clinical manifestations of Cholelithiasis (gallstones)?

A
  • Nausea
  • Pain RUQ, band-like across epigastrium, can radiate to the shoulders
32
Q

Complications of Cholelithiasis (gallstones)?

A
  • Biliary colic (sudden RUQ pain)
  • Chronic cholecystitis
  • Obstructive jaundice…
33
Q

Gold standard diagnosis tool for Cholelithiasis (gallstones)?

A

US

34
Q

Charcot’s triad?

A
  1. High fever
  2. Jaundice
  3. RUQ pain

SURGICAL EMERGENCY: SEPSIS CHOCK RISK

35
Q

Cholestasis?

A

No flow of bile, high ALP and bilirubin, differentials:

  • Primary sclerosing cholangitis: inflammation, NOT infection
  • Biliary pancreatitis
  • Acalculous cholecystitis: ischemic event, no gallstone
36
Q

What is an Haemorrhoid?

A

Is a sinusoid cushion consisting of arterial AND venous blood (non just venous), contribute to 15% continence and may prevent injury to anoderm by hard stools. Types:

  1. Internal
    Above dentate derived from endoderme

3 sites: left lateral, right antero-lateral and right postero-lateral NOT O’clock

  1. External
    Near anal verge, derived from anoderm

Line perianal skin, can thrombose, painfull

37
Q

How do you diagnose hemorrhoids?

A
  1. LOOK (external)
  2. Anoscope/protoscope/retroscope (internal)
38
Q

Treatment of hemorrhoids?

A

Internal (depends on grade):

  • Stool bulking / softeners; warm sitz baths ⇰ symptomatic improvement in 80%
  • NO creams/suppositories
–AVOID straining, prolonged pressures (like reading)

  • Rubber band ligation / sclerotherapy / infrared coagulation (Gr 2,3) –Surgical excision (Gr 3,4)

External:

  • If thrombosed <48h: surgical excision (do not INCISE them!)
  • If >48h: warm sitz baths, stool softeners/bulkers. Clot will reabsorb with time
39
Q

What is an anal Fissure?

A

Is a linear tear in anoderm distal to dentate line. Very painful. Types:

  1. Acute
  2. Chronic: scar, inflamed

LOOK, they are typically in anterior or posterior midline. If it is OFF the midline, need to think about other dx.

40
Q

Treatement of anal fissures?

A
  • Stool bulking agents (water, psyllium, fibber)
  • Sitz baths
  • Topical anesthetics
  • Surgical options: Botox, sphincterotomy
41
Q

Causes of Anorectal abscess & fistula-in-ano?

A
  • IBD/Crohn’s
  • infection
  • trauma
  • surgery
  • neoplasms
  • radiation
42
Q

How do we diagnose Anorectal abscess & fistula-in-ano?

A

we DON’T see it, tender, painful

43
Q

What is the treatment for Anorectal abscess & fistula-in-ano?

A
  • Incision and drainage
  • Warm sitz baths
  • Stool buling
  • Analgesia
  • Consult a surgeon
44
Q

2 anal sphincter and their job?

A
  1. Internal sphincter: smooth, involuntary, resting tone
  2. External: skeletal muscle, voluntary, longitudinal, anoderm
45
Q

Important anal reflexes?

A
  • Gastro-colic: Food in mouth ® colonic motility, segmental contractions
  • Recto-anal inhibitory reflex (RAIR): rectal distension –> RELAXATION of INTERNAL anal sphincter, is it air or stool?
  • Recto-anal excitatory reflex (RAER): rectal distension –> CONTRACTION of EXTERNAL anal sphincter, is that air or stool?
  • Bulbocavernosus reflex: Lowest spinal reflex S2,3,4
46
Q

Risk factors for constipation?

A
  • Increasing age
  • Low-fibber Western diet
  • Decreased physical inactivity
  • Low-income, socio-economic status
  • Limited education
  • History of sexual abuse
  • Depression
  • Medication
47
Q

Players of continence?

A
  1. Internal sphincter
  2. External sphincter
  3. Hemorrhoidal plexus
  4. Functional factors: anorectal angle, puborectalis, flap-valve
48
Q

First cause of incontinence?

A

obstetric complication

49
Q

Management of incontinence?

A
  • It is a symptom, not a diagnosis so treat the underlying cause!
  • Medical management first (bulking, constipating agents, pelvic physical therapist)
  • Surgical options: sphincter reparation, nerve stimulation, colostomy
  • Artificial bowel sphincter
50
Q

Reasons for the high prevalence of chronic diseases today?

A
  1. Epidemiological transition from acute to chronic diseases
  2. Better diagnosis and active searching of chronic diseases
  3. Medicalization (creating new disease categories)
51
Q

We can address chronic disease in 2 approaches, which one?

A
  1. Disease specific
  2. Single comprehensive problem: national institutes of health
52
Q

Management of chronic disease?

A
  • Surveillance
  • Addressing risk factors (1950s)
  • Prevention trough behaviour change
  • When sick, requires new type of treatment management
53
Q

Four mistakes to avoid when talking with patients about risk?

A
  1. Using relative risk (fractions are better)
  2. Using percentage (fractions are better)
  3. Using “1 in X”
  4. Using technical language (say normal test result is better)
54
Q

Steps of shared decision making (SDM)?

A
  1. Step 1: Identify clear decision point
  2. Step 2: Provide information about the options: infographics and decision aids (ADAPTED TO THE LEVEL OF LITTERACY)
  3. Step 3: Elicit patient perspective
  4. Step 4: Guide the patient to a decision
55
Q

Core elements of CDM?

A
  1. Risk communication: Harms & benefits
  2. Values Clarification: What matters most to patients, in terms of outcome?
56
Q

Adenoma to adenocarcinoma pathway?

A
57
Q

Colo-recatal cancer screening guidelines?

A
  • High-risk screening of CRC (≥1 FDR with CRC or advanced adenoma): Start at age 40, intervals depending on no. & age of CRC in FDR (10 years before)
  • Average-risk screening of CRC: start at age 50: screening with FIT every 2 years and sigmoidoscopy every 10 years
  • Only FOBT and flexible sigmoidoscopy have level I evidence supporting use in average-risk CRC screening
  • Low risk of incident proximal CRC and CRC-associated mortality if normal flexible sigmoidoscopy
58
Q
  • Distention of hollow viscus
  • Forceful contractions (biliary and renal colic)
  • Inflammation, ischemia, necrosis

What type of pain?

A

Visceral

59
Q
  • Sharp, stabbing, cutting, localized
  • Usually more sudden onset
  • Aggravated by movement

What type of pain?

A

Parietal/somatic

60
Q

Approach to abdominal pain?

A
  1. ABCs before history/exam for acutely sick patients
  2. Age and gender
  3. PMHx/PSHx

Very important! Do not underestimate

Previous abdominal surgeries – the likelihood of having acute cholecystitis after cholecystectomy is 0, but only if you know that the patient no longer has a gallbladder

  1. Gyne/sexual history
  2. Family history: IBD, AAA
  3. Medications

Recent antibiotics, anticoagulation, anti-reflux rx, steroids, IUD/contraceptives

  1. Pain – OPQRST
  2. Associated symptoms: nausea, vomiting, diarrhea, food, gas, fever, chills, weight loss
  3. Focused review systems: cardiorespiratory, genitourinary, vital signs, general appearance
  4. Inspection
  5. Auscultation
  6. Palpation
  7. Classic signs: Murphy’s, Psoas, Rovsig, McBurney’s point of tenderness
  8. DRE, dimanual speculum exam
  9. Labs: CBC, blood gas, coag profile, liver profile, lipase, troponins, beta-hCG, UA/UC, chem 10
  10. Imaging: X-rays, CT, US (best for biliary pathologies)
61
Q

How can you help prevent T2D?

A
  • There is strong evidence that intensive health behaviour interventions can prevent T2D in adults with prediabetes
  • Use Canrisk questionnaire
  • Prescribe podometer
  • Adress the family (partners influence partners)
62
Q

What is Pancreas Divisum?

A

Failure of ventral & dorsal ducts to anastomose, leads to stenosis of the minor papilla leads to recurrent pancreatitis in 10% - 50% of patients

—-> Endoscopic Retrograde Cholangio-Pancreatogram

63
Q

What is Extrahepatic Biliary Atresia?

A

Biliary tract obstruction and jaundice in first 3 months of life, probably due to failure of the bile ducts to
recanalize

64
Q

What is Choledochal Cyst?

A

Cystic dilation of the common bile duct

65
Q

What are Midgut tragedies?

A

Jejuno-Ileal Atresia: I, II, III, IV

66
Q

What are Hindgut derivations?

A
  • Hirschsprung’s Disease: failure of portion of the hindgut to receive autonomic innervation
  • Cloaca (FEMALE): urorectal septum fuses with cloacal membrane
  • Imperforate anus: high (colostomy) or low (membrane, minor reconstruction)

Bloc E - Final (7 decks)

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