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Clinical Physiology > Diabetes and Diabetes Therapies > Flashcards

Diabetes and Diabetes Therapies Flashcards

1
Q

What is osmotic diuresis?

A

increased urination due to the presence of certain substances in the urine.
caused by high blood sugar and certain medications

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2
Q

Why does diabetes cause weight loss?

A

insulin promotes the uptake of glucose. insulin deficiency causes the body to become catabolic as it thinks its lacking sugar so it breaks down muscle and fat

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3
Q

What type of hormone is insulin?

A

anabolic - synthesises complex structures from products of catabolism

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4
Q

Diabetic ketoacidosis

A

High blood sugar and low insulin results in the liver breaking down fats to form ketones.

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5
Q

DKA is precipitated by__________

A
  • infection, omitting insulin, steroids, MI, CVA , trauma, hyperthyroidism
    • stress response from MI and CVA
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6
Q

What happens during DKA to muscle cells?

A

muscle cells → amino acids → glucose

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7
Q

Gluconeogenesis

A

glucose from macronutrients - protein

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8
Q

Glycogenolysis

A

glycogen → glucose

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9
Q

ketogenesis

A

fatty acids and ketogenic amino acids → ketones

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10
Q

What happens during DKA to fat cells?

A

fat → glycerol and fatty acids
glycerol → glucose
fatty acids → ketones

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11
Q

Symptoms of DKA?

A

PROLONGED HYPERGLYCAEMIA
increased thirst (polydipsia)
increased urination (polyuria)
dehydration

nausea, general malaise, abdominal pain, fruity breath

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12
Q

Why does increased glucose cause polyuria?

A

glucose is an osmotic diuretic

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13
Q

Treatment for DKA

A
  • insulin IV
  • Na water and K loss replaced with IV fluid
  • once ketone <0.6mmol/L and patient eating/drinking convert to subcutaneous insulin
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14
Q

Why is potassium high on first presentation of DKA?

A

due to compensation, acidosis causes potassium to leak from cells into the blood

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15
Q

Steps of Treatment of DKA

A
  1. correct fluid loss
  2. correct hyperglycaemia
  3. correct electrolyte disturbance (specifically potassium)
  4. correct acid-base balance
  5. treat underlying trigger for DKA
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16
Q

Type 1 diabetes

A

inability to produce insulin due to an autoimmune process against pancreatic beta islet cells

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17
Q

Type 3c diabetes

A

insulin deficiency from exocrine pancreatic damage (pancreatitis, pancreatic cancer)

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18
Q

Type 2 diabetes

A

insensitivity to insulin (insulin resistance)

  • associated with obesity
  • associated beta cell dysfunction may be present
  • may develop DKA in acute illness
  • BAME subjects may be ketone prone
19
Q

Effect of insulin deficiency on cells

A

beta cell - produces less insulin
alpha cell - produces excess glucagon → excess sugar production from liver

muscle and fat cells don’t respond to insulin - glucose uptake is low

20
Q

What does measuring faecal elastase tell us?

A

faecal elastase is an exocrine enzyme from the pancreas. If there is an exocrine deficiency it will be low.

21
Q

Complications of Diabetes?

A
  • diabetic retinopathy
  • periodontal disease
  • diabetic nephropathy
  • erectile dysfunction
  • diabetic neuropathy
  • stroke
  • depression
  • heart disease
  • liver disease
  • peripheral vascular disease
  • amputation
22
Q

Why does neuropathy occur in diabetics?

A

damage to small blood vessels supplying the nerves

23
Q

what is an atheroma?

A

fatty material which builds up inside the arteries.

24
Q

Treatment options for type 2 diabetes

A
  • insulin sensitisation
  • insulin replacement
  • insulin secretion
  • lifestyle intervention
  • glucose excretion
25
Q

Insulin sensitisation drugs

A

metformin, pioglitazone

26
Q

Insulin secretion drugs

A

DPP-4 inhibitors (alogliptin, linagliptin)
GLP-1 receptor antagonists (exenatide, liraglutide)
meglitinides (repaglinide, nataglinide)
sulphonylureas (gliclazide, glibenclamide)

27
Q

side effects of metformin and pioglitazone

A

metformin - can accumulate causing risk of lactic acidosis
pioglitazone - increase subcutaneous fat and weight gain

28
Q

Glucose excretion drugs

A

SGLT2 inhibitors:
canagliflozin
dapagliflozin

29
Q

When should metformin not be used?

A

in patients with a GFR < 30ml/min

30
Q

When should SGLT2 inhibitors not be used?

A

in patients with an eGFR<45ml/min

31
Q

How do sulphonylureas work?

A

sugar enters the beta cell to be metabolised into ATP
ATP sensitive potassium channel closes
cell depolarises
depolarisation causes potassium to influx
insulin released

32
Q

Risks of sulphonylureas

A

hypoglycaemia - not glucose sensitive
weight gain

33
Q

How do GLP-1 receptor antagonists work?

A

food ingested
glp-1 released
glp-1 prepares beta cells
promotes insulin secretion
suppresses excess glucagon production
GLUCOSE DEPENDENT

34
Q

How do DPP-4 inhibitors work?

A

DPP-4 breaks down GLP-1
inhibiting this means more GLP-1 is active

can use in renal failure

35
Q

Benefits of GLP-1 receptor antagonists

A

enhanced efficacy
weight loss due to suppressed appetite
cardioprotective
prevents strokes
reduces inflammation in blood vessels
reduce risk of atherosclerosis

36
Q

How do SGLT2 inhibitors work?

A

blood enters the proximal tubule through the glomerulus
sugar absorbed in proximal tubule by SGLT2

in a diabetic, sugar present in urine since sglt2 saturated

an SGTL2 inhibitor reduces the renal threshold so more glucose excreted in urine

37
Q

How do SGLT2 inhibitors reduce BP?

A

increased sodium excretion means reduced BP

38
Q

Why are SGLT2 inhibitors used in heart failure?

A

slight increase in ketone level
ketones are a more efficient fuel for failing heart muscle

39
Q

Risks of SGLT2

A

DKA - therefore contraindicated in type 1 and type 3c patients
increased risk of thrush

40
Q

Why are SGLT2 inhibitors used in kidney disease?

A

kidneys hyperfiltrate sodium and glucose
reduced sodium delivered to macula densa
macula densa dilates afferent arteriole
glomerulus becomes overpressured

the abnormal glucose uptake is caused by SGLT2
inhibition of this causes normal lower reabsorption

41
Q

Modern type 2 diabetes treatment

A
  1. metformin
  2. sglt2 inhibitor (dapagliflozin)
  3. GLP-1 receptor agonist (semaglitude, liraglutide)

SU effective as short term rescue therapy

42
Q

Characteristics of Type 1 Diabetes

A
  • ketone prone due to absolute insulin deficiency
  • more common in childhood
  • associated with other autoimmune disease e.g., underactive thyroid, celiac disease
43
Q

Characteristics of Type 3c diabetes

A
  • ketone prone due to absolute insulin deficiency
  • associated exocrine pancreatic dysfunction e.g, steatorrhea due to deficiency of pancreatic enzymes

Clinical Physiology (11 decks)

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