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Phase 2a Revision > Endo > Flashcards

Endo Flashcards

1
Q

What hormones are released by the anterior pituitary gland

A
  • TSH (thyroid stimulating hormone)
  • ACTH (adrenocorticotropic hormone)
  • FSH & LH
  • GH (growth hormone)
  • Prolactin
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2
Q

What hormones are released by the posterior pituitary gland

A
  • Oxytocin

- ADH (antidiuretic hormone)

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3
Q

What does TSH do

A

stimulates the production of T3 (triiodothyronine) and T4 (thyroxine) from the thyroid gland

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4
Q

What does ACTH do

A

stimulates the production of cortisol by the adrenal gland

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5
Q

What does GH do

A

stimulates the release of insulin-like growth factor 1 (IGF-1) from the liver resulting in

  • muscle growth
  • increases bone density and strength
  • stimulates cell regeneration and reproduction
  • stimulates growth of internal organs
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6
Q

What does oxytocin do

A

stimulates the uterine muscles to contract and also increases production of prostaglandins

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7
Q

what does ADH do

A

acts on the kidney altering the amount of reabsorption that occurs controlling BP via the amount of water in the body

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8
Q

What is the mechanism of the thyroid axis

A

Hypothalamus releases TRH (thyrotropin-releasing hormone) stimulating the anterior pituitary to release TSH, stimulating the thyroid gland to release T3&T4.

T3&T4 cause negative feedback inhibiting the release of TRH and TSH

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9
Q

What is the mechanism of the Adrenal axis

A

Hypothalamus secretes CRH (corticotrophin release hormone) stimulating the anterior pituitary to secrete ACTH which stimulates the adrenal gland to secrete cortisol.

Cortisol has a negative feedback inhibiting the release of CRH and ACTH

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10
Q

How does cortisol work

A

released in pulses from the adrenal glands in response to stressful stimuli. Diurnal variation with conc. varying throughout the day - highest in the morning/lowest in the evening.

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11
Q

What are the different actions cortisol has on the body

A
  • inhibits the immune system
  • inhibits bone formation
  • raises blood glucose
  • increases metabolism
  • increases alertness
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12
Q

How does the growth hormone axis work

A

GNRH is released from the hypothalamus stimulating the anterior pituitary to release GH which stimulates the liver to secrete IGF-1

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13
Q

How does the parathyroid axis work

A

The 4 parathyroid glands secrete PTH (parathyroid hormone) which increased the serum Ca level. Which through negative feedback when the level is to high suppresses the secretion of PTH

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14
Q

How does PTH increase the Ca serum level

A
  • increased the activity and number of osteoclasts in bone causing reabsorption of Ca from bone into the blood
  • stimulates an increase i calcium reabsorption in the kidneys reducing excretion in urine
  • stimulates the kidneys to convert Vit D3 into calcitriol which is the active form of Vit D that promotes Ca absorption from food in the small intestines.
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15
Q

How does the renin-angiotensin system work

A

juxtaglomerular cells that sit in the afferent arterioles in the kidney that respond to low blood pressure by secreting renin, which converts angiotensinogen to angiotensin I, which is then converted into angiotensi II in the lungs via ACE (angiotensin-converting enzyme)

Negative feedback through increase in BP reducing the production of renin

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16
Q

what is renin

A

a hormone/enzyme that acts to convert angiotensinogen to angiotensin I

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17
Q

What does Angiotensin II do

A
  • causes vasoconstriction

- stimulates the release of aldosterone from the adrenal glands

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18
Q

What is Aldosterone

A

mineralocorticoid steroid hormone

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19
Q

what does aldosterone act on

A

nephrons of the kidney

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20
Q

what does aldosterone do

A
  • increase Na reabsorption from the distal tubule
  • increase K secretion from the distal tubule
  • increase hydrogen secretion from the collecting ducts
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21
Q

What is the cause of T1DM

A

insufficient insulin production

22
Q

What is the cause of T2DM

A

insulin resistance

23
Q

what is the normal blood glucose range

A

4.4-6.1mmol/l

24
Q

How does insulin work

A
  • enables cells to absorb and use glucose

- enables muscle and liver cells to absorb glucose and store it as glycogen

25
Q

where is insulin produced

A

beta cells in the islets of Langerhans in the pancreas

26
Q

where is glucagon produced

A

alpha cells in the islets of Langerhans in the pancreas

27
Q

how does glucagon work

A

released in response to low blood sugar levels, stimulates glycogenolysis (breakdown of glycogen to glucose) and glyconeogenesis (production of glucose from proteins and fat)

28
Q

What virus’ are thought to be a potential cause for T1DM

A
  • coxsackie B

- enterovirus

29
Q

Symptoms of T1DM

A
  • thirst,
  • increased urination,
  • recurrent infections,
  • weight loss,
  • drowsiness
  • coma
30
Q

Ix for DM

A
  • HbA1c (>48mmol/mol)
  • random blood glucose (>11mmol/l)
  • fasting glucose (>7mmol/l)
31
Q

How do most T1DM pts initially present

A

DKA

32
Q

what are the main problems in DKA

A
  • dehydration
  • ketoacidosis
  • potassium imbalance
33
Q

what is ketoacidosis

A

where the body carries out ketogenesis due to a lack of usable glucose. Initially the body compensates via the kidneys producing bicarbonate to maintain a normal pH, but eventually the ketone acids use this up causing the blood to become acidotic

34
Q

what causes dehydration in DKA

A

hyperglycaemia causes glucose to be filtered into the urine which draws out water through osmotic diuresis = polyuria = polydipsia

35
Q

why do you get K imbalance in T1DM

A

insulin drives K into the cells. So in T1DM K is not taken up and stored by cells. Serum K may be high or normal but total body K will be low. Therefore when treatment with insulin is started pts can experience severe hypokalaemia = fatal arrhythmias

36
Q

Presenting symptoms in DKA

A
  • polyuria
  • polydipsia
  • N+V
  • acetone smell to breath
  • dehydration = Hypotension
  • altered LoC
37
Q

What is the first priority with DKA Mx

A

fluid resuscitation

38
Q

how to you diagnose DKA

A
  • hyperglycaemia (>11mmol.l)
  • ketosis (>3mmol/l)
  • acidosis (pH<7.3)
39
Q

Mx of DKA

A

FIG-PICK

F- fluid resus with normal saline
I - Insulin
G - glucose (monitor & add dextrose if needed)

P - K (monitor)
I - infection (tx underlying infection)
C - chart fluid balance
K - ketones (monitor ketones or bicarb)

40
Q

Mx of T1DM

A
  • pt education
  • subcutaneous insulin regimes
  • monitoring dietary carbohydrate intake
  • monitoring blood glucose level
41
Q

what types of insulin are typical prescribed

A
  • background
  • long-acting
  • short-acting
42
Q

what complication can be caused by repetitive insulin injections

A

lipodystrophy - where subcutaneous fat hardens preventing the absorption of insulin at that site

43
Q

how can lipodystrophy be prevented

A

cycling the injection site

44
Q

what are the possible short term complications in T1DM

A
  • hypoglycaemia

- hyperglycaemia & DKA

45
Q

Symptoms of hypoglycaemia

A
  • asymptomatic
  • tremor
  • sweating
  • irritability
  • dizziness
  • pallor
  • reduced consciousness
  • coma
  • death
46
Q

Symptoms of hyperglycaemia

A
  • polydipsia
  • polyuria
  • tiredness
  • blurred vision
  • weight loss
  • recurrent infections
  • N&V
47
Q

Mx of hypoglycaemia

A
  • rapid acting glucose (lucozade)
  • slow acting glucose (biscuits/toast
  • IM glucagon
  • IV dextrose
48
Q

Long term macrovascular complications of T1DM

A
  • coronary artery disease
  • peripheral ischaemia disease
  • stroke
  • HTN
49
Q

Long term microvascular complications of T1DM

A
  • peripheral neuropathy
  • retinopathy
  • nephropathy (glomerulosclerosis)
50
Q

Infection related complications of T1DM

A
  • UTI
  • pneumonia
  • skin & soft tissue infections (FEET!!)
  • fungal infections (oral/vaginal candidiais
51
Q

How is T1DM monitored

A
  • HbA1c
  • capillary blood glucose (pts monitor)
  • Flash glucose monitoring (Libra)
52
Q

What is a normal HbA1c

A

48mmol/mol

Phase 2a Revision (13 decks)

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