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gp 3B Flashcards

1
Q

list some risk factors for non alcoholic fatty liver disease

A

METABOLIC SYNDROME- obesity, hypertension, diabetes, hypertriglyceridaemia, hyperlipidaemia

secondary to drugs (NSAIDS, corticosteroids, methotrexate), PCOS, hypothyroidism, hep C virus

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2
Q

Name the stages of non alcoholic fatty liver disease

A

steatosis–> steatohepatitis–> fibrosis–> cirrhosis

insulin resistance leads to build up of fat in liver cells, causes inflammation (steatohepatitis), stellate cells lay down fibrous tissue, and eventually whole architecture of liver is changed (cirrhosis)

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3
Q

signs and symptoms NAFLD

Typical blood test pattern

A

often asymptomatic and picked up incidentally on blood tests

fatigue and malaise. significant damage- hepatomegaly, jaundice, RUQ pain, ascites

LFTs- AST and ALT raised persistently for 3 months
Bigger rise in ALT (L= liver, L=lipids)
(in alcoholic hepatitis AST more raised (s= shit loads of alcohol)

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4
Q

management of NAFLD

A

steatosis and steatohepatits reversible

  • reverse factors causing insulin resistance- diet, exercise, medication to control blood glucose
  • optimise hypertension, hyperlipidaemia, diabetes management

fibrosis and cirrhosis irreversible

  • need for specialist surveillance for hepatocellular cancer (ultrasound scans and AFP
  • liver transplant
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5
Q

diagnosis of NAFLD

A

LFTs
ultrasound scan
biopsy and fibroscan (transient elastography)

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6
Q

complications of NAFLD

A

direct liver complications- portal hypertension, variceal haemorrhage, liver failure, hepatocellular carcinoma, sepsis

metabolic complications- hypertension, CKD, impaired glucose regulation, diabetes type 2

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7
Q

likely cause of LTF results:

raised AST> ALT

A

AST- Cirrhosis or alcohol (Shit loads of alcohol)

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8
Q

likely cause of LTF results:

Raised ALT> AST

A

ALT- acute or chronic liver disease (L=liver specific)

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9
Q

likely cause of LTF results:

raised ALP> ALT

A

ALP- cholestasis (plug)

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10
Q

likely cause of LTF results:

raised ALT> ALP

A

ALT - hepatocellular injury

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11
Q

likely cause of LTF results:

ALP raised, GGT normal

A

ALP, normal GGT- likely bone cause (bp, no GGT in bone)
check calcium

bony mets, primary bone tumour, vit d deficiency, recent bone fracture

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12
Q

likely cause of LTF results:

ALP and GGT raised

A

ALP and GGT- likely liver cause

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13
Q

causes of acute hepatocellular injury

A

paracetamol overdose
infection- hep a, hep B
liver ischaemia

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14
Q

causes of chronic hepatocellular injury

A

alcoholic fatty liver disease
NAFLD
chronic infection (hep B/ C)
primary biliary cirrhosis

(alpha 1 antitrypsin deficiency, wilsons disease haemochromatosis

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15
Q

what are the BMI cut off points

A 
Healthy weight- 18.5-24.9
overweight 25-29.9
obesity 1- 30-34.9
obesity 2 35-39.9
obesity 3- 40 or more
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16
Q

what is the recommended amount of exercise people should do a week

A

30 mins 5 days a week. activities can be in 10 min bursts. 2x weight bearing sessions

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17
Q

summarise the management of type 1 diabetes

A
  • INSULIN- 2x daily background medium acting insulin and pre-meal quick acting insulin
  • monitor blood glucose to determine pre-meal insulin
  • measure carbohydrate intake
  • awareness of blood glucose lowering effect of exercise
  • DAFNE- insulin treatment education programme- dose adjustment for normal eating
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18
Q

summarise the management of type 2 diabetes

A

lifestyle- exercise, diet, weight loss
medication to conrol BP< blood glucose, lipids
identification and prevention of long term microvascular complications

1st line drug treatment- metformin

  • opposes insulin resistance
  • modest improvement in HbA1c
  • no weight gain
  • reduces cardiovascular risk
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19
Q

side effects and risk of metformin

A

diarrhoea, N+V, abdo pain

risk of lactic acidosis if renal function impaired- do not prescribe if eGFR < 30

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20
Q

routine clinical investigations for tired all the time

A 
FBC
ESR and CRP
LFTs
U+E
TFT
glucose/ HbA1c
IgA TTB (coeliac)
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21
Q

what is the risk of using sulphonylurea to treat DM type II

A

hypoglycaemia

weight gain

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22
Q

how should pain management be stepped up in a dying patient

A

WHO analgesic pain ladder

1) non opioid analgesics- NSAIDs, paracetamol
2) weak opioids- cocodamol, codeine, tramadol
3) strong opioids-morphine, fentanyl, methadone, oxycodone

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23
Q

what should be prescribed with an opioid

A

laxatives
softening- docusate
stimulant- senna, bisacodyl

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24
Q

opioid toxicity signs

A

drowsiness, myoclonic jerks, itching, pinpoint pupils, confusion, agitation, cognitive impairment, hallucinations, vivid dreams, respiratory depression

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25
Q

main symptoms to control in dying patient

A 
N+V
breathlessness
respiratory secretions
pain
agitation
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26
Q

what anti-emetic should be used in a patient with parkinsons

A

domperidone- doesn’t cross BBB so cant cause extrapyramidal side effects

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27
Q

5 reversible/ treatable causes of nausea and vomiting

A

drugs- opioids, PPIs, NSAIDs, SSRIs, antibiotics (stop drug)
pain- analgesia
anxiety- explore fears, anxiolytic- lorazepam
constipation- laxatives
raised ICP- dexamethasone
electrolyte disturbances
infection- antibiotic
bowel obstruction- surgery, steroids, antiemetics

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28
Q

Suitable antiemetic for chemical/ drug causes of N+V

A

haloperidol- inhibits chemoreceptor trigger centre

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29
Q

suitable antiemetic for gastric stasis

A

metoclopramide (pro-kinetic agent)

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30
Q

antiemetic used in chemotherapy

A

ondansetron

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31
Q

what is the DS1500 form?

A

form for immediate release of certain funds eg disability living allowance, incapacity benefts etc, for a patient with a terminal illness
fast track to certain welfare benefits

32
Q

pre- emptive medication prescribed for ‘death rattle’

A

hyoscine butylbromide

33
Q

main locations lung cancer metastases to

A 
bone 
brain
liver 
lymph nodes
adrenal glands
34
Q

4 main features of CXR suggesting lung cancer

A

hilar enlargement
peripheral opacity (visible lesion in lung field
pleural effusion- usually unilateral
lobar collapse

35
Q

presentation of AF

A 
asymptomatic
irregularly irregular pulse
syncope/ dizziness
breathlessness
palpitations
chest discomfort
TIA/ stroke
36
Q

pathology of AF

A

irregular atrial rhythm between 300-600bpm.

The AV node is unable to transmit beats as quickly as this, and thus does so intermittently, resulting in an irregular ventricular rhythm.

This irregular stimulation of the ventricles reduces cardiac output by up to 20%, as well as allowing stasis of blood in the heart chambers.

37
Q

causes of AF

A

cardiac- hypertension, heart failure, MI, valve disease, congenital heart disease

pulmonary- PE, pneumonia, bronchocarcinoma

other- alcohol, hyperthyroidism, sepsis, hypokalaemia, hypermagnesaemia

38
Q

ECG findings in AF

A

irregular QRS complexes/ R-R intervals

absent P waves

39
Q

investigations of AF

A

ECG
bloods- U+Es, TFTs, cardiac enzymes
echo- structural abnormalities

40
Q

management of acute AF

A

emergency electro-cardioversion if haemodynamically unstable

if haemodynamically stable
-rate control- betablockers, then digoxin
-rhythm control- pharmalogical cardioversion (amiodarone, flecainide)
anticoagulation- heparin

41
Q

management of chronic AF

A

rate control

  • betablocker (CCB if asthma) 1st line
  • digoxin monotherapy only if sedentary
  • combination therapy (betablocker, digoxin, diltaziem) if uncontrolled

rhythm control

  • if symptoms continue after rate control
  • cardioversion- electrical/amiodarone

pace and ablate strategy

  • left atrial ablation
  • if permanent atrial fibrillation with symptoms or left ventricular dysfunction thought to be caused by high ventricular rates.

assess stroke and bleeding risk

stop smoking, limit caffeine and alcohol

42
Q

how to assess stroke risk in AF

A

CHA2DS2 VASc

1 year risk of stroke

congestive heart failure
hypertension
age >75
diabetes
stroke/ TIA/ TE
Vascular disease
age 65-75 
sex (female)

1- low- moderate risk, consider antiplatelet or anticoagulation
2+ moderate-high risk- start anticoagulant

43
Q

how to assess the risk of bleeding in those starting anticoagulation for AF

A

HASBLED

risk of major bleeding for patients on anticoagulant

Hypertension
abnormal liver/ renal function
stroke
bleeding history/ predisposition
labile INR
elderly >65
drugs/ alcohol

3+ high risk of bleeding

44
Q

if patients were at a high risk of stroke, how could this be managed?

A

anticoagulation

apixaban, rivaroxaban, warfarin, dabigatran

45
Q

risk of stroke following TIA

A

ABCD2 score

age >60
BP > 140/90
clinical features- unilateral weakness (2), speech difficulties (1)
duration (>60 mins (2), 10-59 min (1) )
diabetes
46
Q

definition of CKD

A

reduction in kidney function or structural damage (or both) present for more than 3 months, with associated health implications.

  • eGFR <60mL/min
  • > 3 months
  • evidence of structural/ functional abnormalities: proteinuria, ultrasound, biopsy, U+Es
47
Q

risk factors of CKD

A 
diabetes
hypertension
smoking
AKI
chronic use of NSAIDS
Cardiovascular disease
48
Q

causes of CKD

A

diabetes

pre-renal- renal artery stenosis

renal- diabetic nephropathy, hypertension, glomerulonephritis, myeloma, polycystic kidney disease

post renal- urinary obstruction (enlarged prostate, stone, neurogenic bladder, constipation)

49
Q

presentation of CKD

A

asymptomatic

Ureamic state:
anorexia
loss of appetite
nausea
oedema
muscle cramps
peripheral neuropathy
pallor 
hypertension
nocturia and polyuria
restless legs
amenorrhoea
50
Q

who to screen for CKD

A 
diabetes
hypertension
cardiovascular disease
structural renal disease
recurrent UTIs
SLE
FHx
51
Q

investigations of CKD

A

UEs –> eGFR
eGFr- 2 tests 3 months apart
urine dipstick- haematuria/ proteinuria
FBC- normochromic, normocytic anaemia- anaemia oc CKD (decreased erythropoietin production

early morning urine sample- albumin creatine ratio
BMI, glucose, lipid, BP profile
renal tract ultrasound
kidneys often small

52
Q

CKD complications

A

ABCDEF
Anaemia
blood pressure
calcium phosphate loading + cardiovascular disease
vit D- poor bone metabolism- renal bone disease
electrolyte derangements- acidosis, hyperkalaemia
fluid overload- pulmonary oedema

53
Q

management of CKD

A

identify and treat reversible causes
limit progression/ complications
-BP- ACE-I
-renal bone disease- check PTH, vit D analogues and calcium supplements
-cardiovascular risk- statin, aspirin
-diet- mdt involvement
symptom control
-anaemia- give iron/ b12/ folate and human epo
-acidosis- give sodium barcarbonate
-oedema- loop diuretics, fluid and sodium restriction

renal replacement therapy

54
Q

red flags of a vomiting child

A

not keeping down any food- pyloric stenosis, intestinal obstruction
-projectile vomiting- pyloric stenosis
-bile stained vomit- intestinal obstruction
-haematemesis or melaena- peptic ulcer, oesophagitis
-abdo distension- intestinal obstruction
-reduced consciousness, bulging fontanelle, neurologic signs- meningitis
-respiratory symptoms- aspiration, infection
blood in stool- gastroenteritis, cow milk protein allergy
-rash, angioedema- cows milk protein allergy

55
Q

common causative agents of gastroenteritis

A

norovirus, rotavirus, ecoli, salmonella

56
Q

signs and electrolyte disturbance of pyloric stenosis

A

projectile vomiting, no bowel movements

olive shaped mass RUQ, peristaltic waves L-R dehydration

metabolic alkalosis- hypochloraemic, hypokalaemic

management: correct electrolyte disturbances. Pylomyotomy

57
Q

premature baby, distended stomach, vomited, temperature, refusing feeds, green vomit, fresh blood in stools

likely diagnosis

A

nec- necrotising enterocolitis

diagnosis: transilumination of abdo
AXR: distended loops of bowel, thickened bowel wall, intramural gas, gas in portal venous tract

58
Q

signs of appendicitis

A 
colicky pain getting worse
vomiting
pain moving across abdo
pain relieved by lying still
pyrexic
tenderness and guarding

abdo ultrasound- thickened non-compressible appendix with increased blood flow

59
Q

management of GORD

A

small frequent meals
burping regularly to help milk settle
not over feeding
keep baby upright after feeding

if problematic cases (chronic cough, hoarse cry, distress, reluctance to feed, poor weight gain

  • Gaviscon mixed with feeds
  • thickened milk formula
  • ranitidine- histamine 2 blocker- recued amount of acid stomach produces
60
Q

risk factors of cows milk protein allergy

A

atopy
formula fed
<1yo

61
Q

clinical features of IgE mediated cows milk protein allergy

A

symptoms within 2 hrs of milk consumption
• Skin reactions including itching, erythema, urticaria and acute angioedema
• Colicky abdominal pain, nausea, vomiting and diarrhoea
• Nasal itching, sneezing, rhinorrhoea and congestion
• Cough, chest tightness and wheeze
• Anaphylaxis can occur but is extremely rare

62
Q

clinical features of non- igE mediated cow milk protein allergy

A

symptoms up to a week after ingestion
• Atopic eczema, itching and erythema
• Colicky abdominal pain, reflux, blood or mucus in stool, constipation or diarrhoea
• Cough, wheeze, breathlessness or chest tightness
• Tiredness, weight loss and faltering growth

63
Q

management of cows milk protein allergy

A

-skin prick/ blood test for IgE
-trial exclusion of cows milk (exclude from mums diet of breast fed)
-hydrolysed milk formula
-paediatric dietician
-remission rate high- challenge every 6-12 months
milk alternatives- avoid soya (common allergen), others can be used age 2yo+

64
Q

what is lactose intolerance

A

inability to digest lactose due to lack of enzyme lactase. problem of older childhood and adults

bloating, diarrhoea, gas

not an allergy

65
Q

presentation of cluster headache

management

A 
disabling, rapid onset
excruciating pain around one eye
blood shot, lid swelling, miosis, ptosis, lacrimation
unilateral pain
worse at night
can wake person up
attacks last 15-90 mins, can have several in day
bouts can go on for months, then relapse

management
ACUTE- 200% o2 and sumitriptans
prophylaxis- verapamil

66
Q

presentation of trigeminal neuralgia

A 
Asian male >50
paroxysms of intense stabbing pain, lasting seconds
unilateral
face screws up with pain
electric shock in jaw/teeth/gums
triggers eg washing hair, brushing teeth

management: carbamazepine

67
Q

presentation of migraine

management

A 
vomiting
photophobia
aura
triggers
FHx

management

  • acute- triptans, nsaids, paracetamol, anti emetics
  • chronic- propranolol, topiramate
68
Q

presentation of GCA

A

> 50 headache, lasting a few weeks
tender thickened pulseless temporal arteries
jaw claudication
ESR >40

treatment: steroids

69
Q

metabolic causes of itch

A

chronic renal failure and dialysis, liver disease, cholestasis
-uraemic pruritic

70
Q

haematological causes of itch

A

iron deficiency anaemia- do FBC (glossitis, angular cheilitis)
polycythaemia rubravera- itching after hot bath. Red face, splenomegaly, burning sensation in fingers and toes, dizziness tinnitus (JAK2 mutation)

71
Q

endocrine causes of itch

A

graves disease

diabetes mellitus- increased risk of candida infection

72
Q

paraneoplastic causes of itch

A

lymphoma (not usually leukaemia)

especially hodgkins lymphoma

73
Q

Presentation of seborrheic dermatitis

management

A

chronic relapsing remitting

scalp, face and trunk
oily skin, psoriasis, immunosuppression, stress

oily and dry skin, scaly patches, scaly red eyelid margins (blephitis), flaky patches around hair line, salmon pink think scaly patches

Mx- antifungal- ketoconazole

74
Q

investigating systemic causes of itch

A 
fbc
esr
serum ferritin
WCC
FBC
LFTs
renal function and electrolytes
thyroid function tests
75
Q

signs of drug dependency syndrome

A

craving
difficulty controlling substance use
withdrawal state
tolerance
progressive neglect of pleasures and interests
persistent use despite clear evidence of harmful consequences

guilt, keeping drug use secret, arguments

GP 3b (1 decks)

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