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Phase 2 > Phase 2 Exam Content > Flashcards

Phase 2 Exam Content Flashcards

1
Q

What is the natural progression of colorectal cancer?

A

AK53

Loss of function of APC tumour suppressor leading to early adenoma, gain of function of KRAS causing unregulated cell growth and proliferation, loss of function of TP53 tumour suppressor causing progression from adenoma to adenocarcinoma.

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2
Q

What is the most common type of colorectal cancer?

A

Adenocarcinoma

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3
Q

What are modifiable and non-modifiable risk factors for colorectal cancer?

A

Modifiable:

  • smoking
  • low-fibre diet
  • obesity
  • processed meats

Non-modifiable:

  • age
  • hereditary polyposis syndromes
  • positive family history
  • IBD
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4
Q

What is the TNM staging of CRC?

A

T1- through submucosa
T2- through muscularis propria
T3- pericolorectal tissues
T4- into peritoneum

N1- 1-3 regional lymph nodes
N2- 4-6 regional lymph nodes

M0- nothing
M1- 1 site
M2- 2 sites

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5
Q

What is the prognosis for CRC?

A 
Duke's A: T1N0M0: 95%
Duke's B1: T2N0M0: 85%
Duke's B2: T3N0M0: 70-80%
Duke's C: TxN1M0: 35-65%
Duke's D: TxNxMx: 5%
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6
Q

What is prevalence?

A

The number of prevalent cases is the total number of cases of disease existing in a population.

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7
Q

What is incidence?

A

Incidence is the number of newly diagnosed cases of a disease.

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8
Q

What is mortality rate?

A

The number of deaths in a given area or period, or from a particular cause.

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9
Q

What epithelium are the majority of anal cancers?

A

Squamous cell cancers

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10
Q

What are the classic findings of small bowel obstructions?

A

Dilated, air-filled, small loops of bowel with relatively little gas in bowel.

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11
Q

What are the most common causes of small bowel obstructions in adults?

A

Adhesions (60%), hernias (10-20%), neoplasms (10-20%), intussusception, gallstone, ileus, stricture secondary to IBD, volvulus

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12
Q

What if the most common cause of small bowel obstruction in children?

A

Hernia

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13
Q

What is the initial management of small bowel obstruction?

A
  • Fluid resuscitation
  • NPO status
  • pain management (avoid opioids and anticholinergics)
  • IV hydration
  • Foley catheterisation
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14
Q

What on history suggests infective diarrhoea?

A

Acute onset
Duration less than two weeks
Self-limiting
Exposure (travel, food, etc)

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15
Q

What are conditions that mimic diarrhoea?

A
  • overflow incontinence
  • laxative use
  • incontinence
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16
Q

What are the risk factors and treatment for salmonella?

A

Risk factors: consumption of contaminated poultry or eggs, affects young or old more frequently

Treatment: Fluids or oral quinalone in high risk patients

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17
Q

What are risk factors and treatment for C.Diff?

A

Risk factors: recent antibiotic treatment, hospitalisation

Treatment: stop antibiotics, PO metronidazole for mild, PO vancomycin for moderate

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18
Q

What are risk factors and treatment for Norovirus?

A

Risk factors: childcare, contaminated food, travel

Treatment: Fluids

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19
Q

What are risk factors and treatment for Cryptosporidium?

A

Risk factors: contaminated water, childcare, travel

Treatment: supportive

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20
Q

What are non-infective causes of diarrhoea?

A
  • IBS
  • IBD (ulcerative colitis or Crohn’s)
  • Diverticulitis
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21
Q

What are four functions of the GI tract?

A

Motility, digestion, absorption and secretion.

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22
Q

Questions for paeds history of constipation?

A 
When did it start?
Initially pooing or suddenly stopped?
Passing gas? 
Fever?
Feeding? 
Unsettled? 
Vomiting?
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23
Q

What are signs of congenital hypothyroidism?

A
  • Constipation
  • Fatigue and lethargy
  • Poor appetite
  • Prolonged jaundice
  • Poor growth
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24
Q

What does the Guthrie test look for and how?

A

CF- immunoreactive trypsinogen
Congenital hypothyroidism- TSH or T4
CAH- 17OHP
PKU- Phenylalanine

25
Q

Major Depressive Disorder Features

A

5/9 symptoms for greater than 2 weeks- one of first two

2

  • low mood
  • anhedonia

3

  • suicidal ideation
  • poor concentration
  • guilt

4 SAME

  • sleep disturbance
  • appetite
  • motor
  • energy
26
Q

BPD Features

A

5 symptoms since adolescence, inflexible across multiple environments

Abandonment 
Mood instability
Suicidal ideation
Unstable relationships  
Impulsivity 
Control of anger (poor)
Identity disturbances
Dissociation 
Empty feelings
27
Q

BPAD Features

A

Symptoms of mania

Distractibility
Insomnia 
Grandiosity 
Flight of ideas 
Activities/Agitation
Sexual disinhibition
Talkativeness

BPAD 1: manic episode
BPAD 2: hypomanic, more than one MDD episode
Cyclothymic: does not meet criteria for hypomania or MDD but alternating symptoms for two years

28
Q

PTSD Features

A

Symptoms for > 1 month

Intrusive symptoms: nightmares and flashbacks
Avoidance: stimuli associated with trauma
Negative alterations in mood and cognition: numb
Changes in arousal and reactivity: hypervigilance, sleep disturbances

29
Q

Substance Use Disorder Features

A

2/11 criteria for 1 year

Social impairment

  • work/school/home
  • continued despite problems
  • isolation

Impaired control

  • more consumption than intended
  • failed reduction
  • increased time spent acquiring
  • craving

Risky use

  • hazardous situations
  • continued despite issues

Pharmacologic

  • tolerance
  • withdrawal
30
Q

Schizophrenia Features

A

> 6 months symptoms

Delusions
Hallucinations
Speech (disorganised)

Behaviour (disorganised)
Negative symptoms (affect, avolition, asociality, anhedonia, apathy)
31
Q

Presentation of RPOC

A

uterine bleeding, pelvic pain, fever, uterine tenderness

32
Q

Complication of RPOC

A 
Sepsis 
Haemorrhage
Cervical stenosis 
Cervical incompetence 
Adhesions 
Vaginal bleeding
33
Q

Medical management of RPOC

A

Vaginal misoprostol

SE: Abdominal cramping, diarrhoea, vaginal bleeding, nausea, vomiting

34
Q

Antiphospholipid syndrome effects

A 
Coagulation defect
Livedo reticularis 
Obstetric
Thrombocytopaenia
SLE
35
Q

Antiphospholipid syndrome diagnostic criteria

A

Clinical (one needed)

  • vascular thrombosis
  • pregnancy morbidity

Labs (one needed) 12 weeks apart

  • anticardiolipin antibody
  • lupus antibody
36
Q

Antiphospholipid syndrome and pregnancy

A
  • increased risk of developing a thrombosis and miscarriage
    -at risk for preeclampsia and decreased blood flow to the foetus resulting in intrauterine growth restriction
    -manage with:
    low dose aspirin
    heparin
    stop warfarin when trying to conceive
    no COCP because oestrogen and increased risk of clots
37
Q

Causes of recurrent miscarriages

A

Chromosomal abnormalities (early before 12 weeks)
Anatomical abnormalities of the uterus
Endocrine disorders (DM, hypothyroidism)
Other inherited thrombophilia (Factor V leiden, protein C and S)
Antiphospholipid syndrome
Late spontaneous miscarriage (12-20 weeks) due to hypercoagulable state

38
Q

Cough history

A 
When did it start?
Can you cough for me?
Are you producing any sputum?
Have you coughed up blood? 
Has it gotten better or worse? 
Anything that helps or makes worse? 
Smoke?
Fevers, night sweats, weight loss?
Occupational exposure?
Travel?
Pets?
39
Q

Examination findings pleural effusion

A

Dullness to percussion
Decreased tactile fremitus
Asymmetrical chest expansion

40
Q

SIADH Causes

A

Central or nephrogenic

  • pulmonary disease
  • paraneoplastic syndrome
  • tumour
  • drugs: antipsychotics, NSAIDs
41
Q

Multiple myeloma features

A

Hypercalcaemia
Renal involvement
Anemia
Bone lesions

42
Q

Differential diagnosis for jaundice

A

Pre hepatic

  • increased haemolysis (malaria, HUS, etc)
  • decreased conjugation (crigler najaar, gilberts, etc)

Intrahepatic
Hepatitis
Cirrhosis

Post hepatic
Choledocolithiasis
Pancreatic malignancy

43
Q

What are the clinical signs of liver failure?

A 
Jaundice
Ascites 
Coagulopathy 
Disorientation or confusion 
Pruritis 
Dark urine 
Pale stools
44
Q

Functions of the liver and how dysfunction results in symptoms

A

Synthetic function:
Clotting factors –> coagulopathy
Proteins–> ascites

Clearance of toxins:
Ammonia –> hepatic encephalopathy
Bilirubin –> jaundice

45
Q

What are the components of child pugh classification for liver failure?

A 
Bilirubin
Albumin 
PT INR
Ascites
Hepatic encephalopathy

-lower score means higher chance of one year survival, there are classes A, B, and C

46
Q

What are the consequences of chronic hepatitis?

A

Cirrhosis, portal hypertension, liver failure, and hepatocellular carcinoma

47
Q

What is the goal for treatment of cirhosis?

A

Stop progression and prevent complications

48
Q

What is cirrhosis?

A

Fibrosis and nodular regeneration resulting from chronic hepatic injury. Most commonly caused by alcohol, chronic viral infection (HCV), and non alcoholic steatohepatitis

49
Q

What are the complications of cirrhosis?

A

Ascites: increased portal hypertension causes transudative effusion, manage with sodium restriction and diuretics

SBP: paracentesis >250 PMNs/mL, IV Abx acutely, I albumin

Hepatorenal syndrome: “healthy kidneys in an unhealthy environment”

Hepatic encephalopathy: decreased clearance of ammonia, lactulose

Oesophageal varices: portal hypertension leads to increased flow through porto-systemic anastamoses, acute bleeding > endoscopy with band ligation or sclerotherapy, TIPS in refractory cases but associated with poor outcome, beta blockers can be used prophylactically

Coagulopathy: impaired synthesis of all clotting factors except VIII, for acute bleeding fresh frozen plasma

50
Q

Cholelithiasis (DIASG)

A

Definition: stones in gallbladder causing temporary occlusion

Presentation: Asymptomatic or biliary colic, transient RUQ pain after eating fatty meals

Labs: normal bilirubin, ALP, amylase

Dx: US

Mx: observation if asymptomatic, laparoscopic cholecystectomy if symptomatic

51
Q

Kawasaki disease

A
  1. fever for more than 5 consecutive days
  2. palmar erythema
  3. head and neck rash
  4. cervical lymphadenopathy
  5. conjunctival congestion
  6. strawberry tongue
Conjunctival
Rash
Edema 
Adenopathy
Mucosal involvement
52
Q

Kawasaki treatment

A

IV immunoglobulins

53
Q

Diagnostic criteria PCOS

A

-oligo/anovulation
-hyperandrogenism
clinical (hirsutism or less commonly male pattern alopecia) or
biochemical (raised FAI or free testosterone)
-polycystic ovaries on ultrasound

54
Q

Ddx PCOS

A 
Congenital adrenal hyperplasia 
Androgen secreting tumours 
Cushing syndrome
Thyroid dysfunction 
Hyperprolactinaemia
55
Q

Investigations for PCOS

A 
Testosterone
FSH/LH
OH-17 for CAH
BSL
HbA1C
TFTs
Prolactin
56
Q

Management of PCOS

A

Not trying to conceive: COCP or Progestin + metformin

Trying: Clomiphene (SERM) plus metformin

Symptoms:

57
Q

Simple versus complex ovarian cysts on ultrasound

A

Simple cysts: anechoic, thin wall, smooth, reduced or no blood flow

Complex: Vascular, echoic, septate, thick wall irregular walls

58
Q

Types of ovarian cysts

A

Functionals: follicular and corpus luteal

Non-functional:
Dermoid
Chocolate cysts (endometriosis)
Haemorrhagic

Neoplasms:
epithelial (90%) CA-125

59
Q

Ovarian torsion

A

Aetiology: hypermobile ovary (50%) or adnexal mass

Presentation: severe non-specific lower abdominal and pelvic pain, either intermittent or sustained, nausea, and vomiting. There is an adnexal tenderness. A raised white cell count is common.

Imaging: The main feature of torsion is ovarian enlargement due to venous/lymphatic engorgement, oedema, and haemorrhage. Secondary signs include free pelvic fluid, an underlying ovarian lesion, reduced or absent vascularity and a twisted dilated tubular structure corresponding to the vascular pedicle.

Phase 2 (1 decks)

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