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Med 4 > ITM The Middle Aged Patient > Flashcards

ITM The Middle Aged Patient Flashcards

1
Q

What is the difference between T1 and T2 diabetes

A

T1: body cannot produce any insulin due to a genetic predisposition to autoimmune pancreatic B cell destruction
T2: there is not enough insulin due to impaired B cell function

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2
Q

Define insulin resistance

A

The organs and tissues of the body lose their sensitivity to the action of insulin

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3
Q

What is insulin resistance triggered by

A

Chronically: overweight / obesity and physical inactivity
Acutely: infection / trauma / injury / pregnancy

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4
Q

What is the diagnostic criteria for T2 diabetes

A

Fasting glucose >7 mmol/l
Blood glucose of >11.1 mmol/l after a 2 hour oral glucose tolerance test
HbA1c level >48 mmol/mol

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5
Q

What are the microvascular complications of DM

A

Eyes
Kidneys
Peripheral nervous system

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6
Q

What are the macrovascular complications of DM

A

Stroke and MI

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7
Q

What is metabolic syndrome

A

A cluster of risk factors for cardiovascular disease and T2 DM

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8
Q

What are the risk factors for metabolic syndrome

A

Central obesity (88cm female, 104cm men)
Triglycerides >1.7mmol/l (usual is 1 mmol /l)
HDL cholesterol <1 mmol/l males, <1.3mmol/l female
Blood pressure >130/85 mmHg
Fasting glucose >5.6mmol/l
Presence of ectopic fat (liver, pancreas, skeletal muscle)

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9
Q

What causes insulin resistance

A

High dietary fat availability
Adiposity - ectopic fat accumulation
Physical inactivity (2-3 days of bed rest can cause insulin resistance)

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10
Q

What are the 2 components of pre diabetes

A

Impaired fasting glucose (IFG) and / or impaired glucose tolerance (IGT) markedly increase the risk of developing T2D

If not reversed the rate of conversion to T2D is 5-10% per annum
Healthy HbA1c is <38mmol/mol; T2D >48 mmol/mol

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11
Q

What are impaired fasting glucose and impaired glucose tolerance

A

IFG = fasting glucose >5.6mmol/l - <7mmol/l (when the liver is less sensitive to insulin it pumps out more glucose)

IGT= blood glucose of >7.8mmol/l - <11.1mmol/l after a 2 hour oral glucose tolerance test

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12
Q

Define pain

A

A highly unpleasant physical sensation caused by illness or injury

An unpleasant sensory and emotional experience associated with actual or potential tissue damage or described in terms of such damage

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13
Q

Define acute abdominal pain

A

Previously undiagnosed abdominal pain that arises suddenly and is of less than 7 days and usually less than 48h duration

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14
Q

3 classifications of abdominal pain

A

Visceral: crampy, achy, diffuse, poorly localised

Somatic: sharp, cutting, stabbing, well localised

Referred: distant from site of generation, symptoms but no signs

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15
Q

Surface anatomy of the foregut, midgut and hindgut

A

Epigastric region: foregut
Periumbilical region: midgut
Pelvic region: hindgut

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16
Q

Does psoriasis increase cardiovascular risk

A

Slight increased risk due to inflammation inside the body which can eventually affect the heart and blood vessels

17
Q

Post operative causes of abdominal pain

A

Intra-abdominal bleeding or collection, anastomotic leak / dehiscence
Abdominal compartment syndrome

18
Q

Pulmonary causes of abdominal pain

A

Lobar pneumonia
Pleurisy (inflammation of pleura between lungs and ribs)
Pulmonary embolism

19
Q

Cardiac causes of abdominal pain

A

Acute MI
Congestive cardiac failure
Myocarditis

20
Q

Metabolic / endocrine causes of abdominal pain

A 
Porphyria
Diabetic keotacidosis 
Lead poisoning 
Hypercalcemia 
Adrenal insufficiency
21
Q

Vascular causes of abdominal pain

A

Henoch-schonlein purpura
Systemic lupus
Polyarteritis nodosa
Familial Mediterranean fever

22
Q

When is the location and severity of abdominal pain altered

A

Pregnancy
The older adult
Immunocompromised patients
Altered anatomy eg malrotation, sinus inversus

23
Q

What is methotrexate and how is it prescribed

A

Methotrexate is a drug used for immunocompromised patient eg with rheumatoid arthritis. It is prescribed weekly as it is seen to be less hepatotoxic when given weekly

24
Q

When are beta blockers contraindicated

A

In patients with asthma or COPD due to their increased probability of causing bronchospasm

25
Q

What is the caution with ACE inhibitors

A

Start with a low dose and adjust according to response. Hyperkalaemia and other side effects of ACE inhibitors are more common in those with impaired renal function and the dose may need to be reduced

26
Q

Risk of ACE inhibitors and pregnancy

A

ACE inhibitors should be avoided in pregnancy unless essential
May adversely affect fetal and neonatal blood pressure control and renal function; skull defects and oligohydraminos have also been reported

27
Q

Different routes of administering drugs

A 
Po: oral 
Im: intramuscular 
Iv: intravenous 
Sc: subcutaneous 
Neb: nebuliser 
Sl: sublingual (under tongue) 
ih: inhalation
28
Q

Why does psoriasis increase cardiovascular risk

A

Because if there is long term inflammation is can eventually harm the heart and blood vessels

29
Q

When can preventative metformin be given

A

If the patient is unable / unwilling to change their lifestyle factors

30
Q

What is acute pancreatitis

A

A condition in which the pancreas becomes inflamed over a short period of time
Usually heals within a week

31
Q

What investigations would you run if acute pancreatitis is suspected

A

Blood tests to measure 2 digestive enzymes: amylase and lipase. If the levels are high then acute pancreatitis is likely

32
Q

Underlying causes of acute pancreatitis

A 
Drinking 
Steroid treatment (psoriasis) 
Gall stones 
Metabolic disorders 
Infections
33
Q

How is acute pancreatitis treated

A

Monitored in hospital for signs of serious problems and given fluids and oxygen

34
Q

What does high gamma glutamyl transpeptidase indicate

A

Liver disease or damage to the bile ducts can be caused by drinking

35
Q

Risk factors for developing T2 DM

A 
Obesity 
Age >40 
PCOS 
Black / south Asian ethnicity 
Family history of DM 
Gestational DM 
Physical inactivity 
Dyslipidaemia
36
Q

Complications of DM

A

Micro vascular and macro vascular complications
Diabetic ketoacidosis
Acute hypoglycaemia
Hyperosmolar hyperglycaemic state

37
Q

What is the molecular target for metformin

A

AMP kinase

38
Q

What is the mode of action of a sodium glucose transport inhibitor

A

In a healthy person, glucose is filtered at the renal glomeruli and reabsorbed in the PCT via sodium glucose transporters in the luminal membrane of the tubular cells of the PCT
SGLT 2i block glucose reabsorption leading to glucosuria
And the loss of glucose in the urine leads to lowered blood glucose

Med 4 (12 decks)

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