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NUR5002 > Endocrine > Flashcards

Endocrine Flashcards

1
Q

Thyroid hormones:

A
  • Thyroxine (T4): most abundant
  • Triiodothyronine (T3): more potent
  • Calcitonin: calcium levels

**Iodine required for synthesis of hormones

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2
Q

What systemic effects do thyroid hormones have on the body:

A
  • Metabolic rate
  • Energy requirements
  • Oxygen consumption
  • Carbohydrate and lipid metabolism
  • Growth and development
  • Brain functions
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3
Q

Clinical manifestations of hyperthyroidism

A
  • Goitre
  • Opthalmopathy
  • Exopthalmos
  • HTN
  • Boudning pulses
  • Tachycardia
  • Arrhythmias
  • Increased appetite
  • Loss of weight
  • Splenomegaly
  • Warm, moist smooth skin
  • Thin, brittle nails
  • Hair loss/fine silky hair
  • Fatigue
  • Muscle weakness
  • Osteoporosis
  • Fine tremor
  • Insomnia
  • Personality changes
  • Hepatomegaly
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4
Q

Management of hyperthyroidism

A
  • Antithyroid drugs
  • Iodine
  • Beta-blockers (symptoms)
  • radioactive iodine therapy
  • surgical
  • nutrition
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5
Q

Hypothyroidism causes:

A
  • autoimmune
  • absence of thyroid gland
  • lack of TRH related to a tumour or disorder of the hypothalamus
  • iodine insufficiency
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6
Q

Clinical manifestations of hypothyroidism:

A
  • Exhaustion, lethargy
  • impaired memory
  • slow speech
  • depressed
  • long periods of sleep
  • decreased CO
  • anaemia
  • bruised easily
  • absence/decreased hydrochloric acid
  • decreased GI motility, constipation
  • cold intolerance
  • hair loss
  • dry, course skin
  • brittle nails
  • hoarseness of voice
  • weight gain
  • periorbital oedema
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7
Q

Management of hypothyroidism

A
  • thyroid hormone replacement (adjusted according to response, cardiac side effects)
  • nutritional therapy
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8
Q

Does the thyroid use positive or negative feedback systems

A

Negative

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9
Q

Symptoms of hypoglycaemia:

A
  • blurred vision, drowsiness, ataxia
  • paraesthesia, weakness, muscle spasms
  • tachycardia, palpitations, normal to high BP
  • rapid, shallow respirations
  • diaphoresis, cool and clammy skin
  • urine glucose negative, BGL low
  • anxious, increased stress
  • associated with overdose of insulin or missed meal
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10
Q

Function of the pancreas gland:

A
  • Endocrine gland - produces hormones in the islets of langerhans
  • Exocrine gland - releases sodium bicarbonate and pancreatic enzymes directly into the common bile duct to be released into the small intestine
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11
Q

Metabolic changes when insufficient insulin is released:

A
  • hyperglycaemia
  • glycosuria (glucose in urine)
  • polyphagia
  • polydipsia
  • lipolysis
  • ketosis
  • acidosis (liver cannot remove all waste products)
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12
Q

Disorders associated with diabetes:

A
  • atheroslerosis: heart attacks and strokes related to the development of atherosclerotic plaques in the vessel lining
  • retinopathy: with resultant loss of vision as tiny vessels in the eye are narrowed and closed
  • neuropathies: with motor and sensory changes in the feet and legs and progressive changes in other nerves as the oxygen is cut off
  • nephropathy: with renal dysfunction related to changes in the basement membrane of the glomerulus
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13
Q

Clinical signs and symptoms of hyperglycaemia

A
  • fatigue
  • lethargy
  • irritation
  • glycosuria
  • polyphagia
  • polydipsia
  • itchy skin
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14
Q

Signs of impending dangerous complications of hyperglycaemia:

A
  • fruity breath as the ketones build up in the system and are excreted through the lungs
  • dehydration as fluid and important electrolytes are lost through the kidneys
  • slow, deep respirations (Kussmaul’s respirations) as the body tries to rid itself of high acid levels
  • loss of orientation and coma
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15
Q

Metformin (glucophage)

A
  • first line oral med for T2DM
  • monitor kidney function
  • GI side effects most common
  • starting dose matters for tolerability
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16
Q

Three major complications of DM:

A
  1. Diabetic ketoacidosis (DKA)
  2. Hyperosmolar hyperglycaemia state (HHS)
  3. Hypoglycaemia
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17
Q

What is diabetic ketoacidosis:

A
  • hyperglycaemia because glucose can’t get into cells, therefore cells are starving and break down fats causing ketosis, which eventually results in acidosis
  • severe dehydration and electrolyte imbalance as well
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18
Q

Precipitants of DKA

A
  • usually T1DM
  • change to insulin, diet or exercise
  • Physical/psychological - stress, trauma, surgery
  • Imbalance in the ratio of glucagon and other counter regulatory hormones to insulin
  • Infection
  • Pancreatitis
  • AMI
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18
Q

Metabolic disturbances in DKA

A
  • Hyperosmolarity
  • metabolic acidosis
  • extracellular volume depletion
  • electrolyte imbalances
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18
Q

Clinical manifestations of DKA:

A
  • Polyuria, polydipsia, polyphagia
  • blurred vision
  • weight loss
  • weakness
  • abdominal pain
  • nausea and vomiting
  • acetone breath
  • kussmaul respirations
  • tachycardia
  • hypotension
  • decreased JVP
  • dry mucous membranes
  • ACS - confusion & drowsiness
  • coma
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18
Q

DKA investigations:

A
  • Blood ketones
  • BGLs
  • blood gases (acidotic, decreased bicarbonate, decreased CO2)
  • U&E/creatinine - Na+, K+, LFTs, PO4, Ca2+, Mg2+
  • FBE - WCC
  • Urinalysis
  • Septic workup (MSU, blood cultures, CXR)
19
Q

Management of DKA:

A
  • Identify and correct underlying cause
  • Rehydration and correction of electrolyte losses
  • Correction of hyperglycaemia and acidosis
  • Combination of insulin, fluid and electrolyte balance will correct acidosis
20
Q

Potassium replacement in DKA:

A
  • No K+ in first litre of fluid
  • commence in 2nd litre once K+ level known
  • Check serum K+ prior to each litre of normal saline
  • cardiac monitor if replacement >15mmol
21
Q

Insulin therapy with DKA

A
  • Commence only after fluid resuscitation initiated and serum K+ > 3.5mmol/L
  • IV administration
  • bolus dose
  • Check BGL hourly and adjust infusion according to sliding scale accordingly
  • attempt to keep BGL between 10-15mmol/L at 100mL/hr
22
Q

Glucose therapy after DKA

A
  • Commence IV dextrose when BGL <15mmol at 100ml/hr
  • to prevent rapid decreases in glucose as hypoglycaemia could result in fatal cerebral oedema
  • run concurrently with normal saline
23
Q

Other management of DKA

A
  • oxygen therapy
  • hourly urine and strict FBC
  • cardiac monitoring (ECG)
  • septic workup (CXR, MSU, blood cultures)
  • bloods
  • focal signs of infection
  • NBM first 24hrs
  • frequent obs
  • avoid sedation
24
Q

What is a hyperosmolar hyperglycaemic state (HHS)?

A
  • SImilar to DKA but the critical differences are:
  • degree of insulin deficiency
  • degree of fluid deficit
  • absence of ketone production
  • onset usually days to weeks whereas DKA is rapid
  • not ketotic
25
Q

Causes of hyperosmolar hyperglycaemic state (HHS):

A
  • infection and other acute illnesses, often cardiovascular
  • drugs such as beta blockers, calcium channel blockers and diuretics
26
Q

Patient characteristics of hyperosmolar hyperglycaemia state (HHS):

A
  • patients tend to be older and sicker
  • consider pre-existing illness
  • higher mortality rate than DKA
27
Q

Hyperosmolar hyperglycaemic state (HHS) treatment:

A
  • insulin therapy may not be required (only commenced after rehydration)
  • ketone level is normal or only mildly elevated as enough circulating insulin to prevent ketoacidosis
  • severe electrolyte imbalance
28
Q

Hyperosmolar hyperglycaemic state (HHS) clinical manifestations:

A
  • severe dehydration: 5-12L deficit
  • significant hyperglycaemia: good glucose level >34mmol/L
  • renal failure as kidneys cannot excrete glucose further contributing to hyperglycaemia
  • severe hypernatraemia: loss of water > loss of Na+ = hypertonic dehydration
29
Q

Hyperosmolar hyperglycaemic state (HHS) management:

A
  • DRSABCD
  • Neurological assessment
  • FBE, U&Es/Cr, BGL, blood ketone, ABG
  • fluid resuscitation
  • electrolyte replacement
  • +/- insulin administration
  • ECG + cardiac monitoring
  • IDC
  • septic workup
30
Q

Causes of hypoglycaemia:

A
  • mismatch in timing of food and peak action of insulin or oral hypoglycaemia agents that enhance endogenous insulin production
  • too much insulin or medication
  • ingestion of too little food
  • delaying time of eating
  • performing unusual amounts of exercise
    may also occur when very high glucose is brought down too rapidly
31
Q

Acute complications of diabetes:

A
  • hypoglycaemic shock
  • hyperglycaemic hyperosmolar state
  • diabetic ketoacidosis
32
Q

Chronic complications of diabetes:

A
  • Stroke, atherosclerosis
  • cataracts, retinopathy
  • MI, arrythmias
  • nephropathy and kidney infection
  • neuropathy (impotence and infertility, urinary incontinence, autonomic neuropathy)
  • peripheral neuropathy (numbness, weakness)
  • peripheral vascular disease (foot ulcers, delayed healing, gangrene)
33
Q

HbA1C (glycosylated haemoglobin)

A
  • measures average BGL over 2-3months
  • <7% greatly reduces risk of developing microvascular complications
  • non-diabetic normal range = 3.5-6%
34
Q

Glucose excreted in the urine

A

Glucosuria

35
Q

Clinical syndrome of hypermetabolism

A

Thyrotoxicosis

36
Q

What is the importance of BGL monitoring in the fasting patient

A

to monitor for hypotension

37
Q

how frequently should BGL monitoring be performed on the fasting patient

A

hourly

38
Q

Clinical manifestations of hyperthyroidism:

A
  • sweating
  • startled facial expression
  • palpitations
  • tachycardia
  • flushed skin
  • tremor
  • hyperexcitable
39
Q

Clinical manifestations of hypothyroidism:

A
  • coldness
  • expressionless face
  • weight gain
  • personality changes
  • hair loss
  • hoarse voice
  • fatigue
40
Q

Clinical manifestations of hypoglycaemia?

A
  • confusion
  • tachycardia
  • drowsiness
  • palpitations
  • pallor
  • sweating
  • irritability or anxiety
  • slurred speech
41
Q

hypoglycaemia treatment

A
  • glucose injection
  • glucagon injection
  • eating/drinking carbohydrates
42
Q

Clinical manifestations of hyperglycaemia:

A
  • nausea
  • acidosis (DKA)
  • polyphagia
  • polydipsia
  • ketosis
  • dehydration
  • weakness
  • polyuria
43
Q

Main functions of steroid hormone cortisol?

A
  • decrease inflammatory cytokines
  • increasing hepatic glucose production
44
Q

Prolonged use of steroids such as prednisolone may lead to:

A

Cushing’s syndrome

45
Q

Hyperosmolar hyperglycaemic state/syndrome (HHS) normally occurs in which type of diabetes

A

Type 2

46
Q

What do thyroid hormones impact in the body:

A
  • metabolic rate
  • energy requirements
  • oxygen consumption
  • carbohydrate and lipid metabolism
  • growth and development
  • brain functions
47
Q

Inner medulla of the adrenal glands produce which hormones:

A
  • adrenaline and noradrenaline
48
Q

Outer cortex of adrenal glands produce which hormones:

A
  • corticosteroid hormones (mineralocorticoids, glucocorticoids)

NUR5002 (10 decks)

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