Endocrine Flashcards
Thyroid hormones:
- Thyroxine (T4): most abundant
- Triiodothyronine (T3): more potent
- Calcitonin: calcium levels
**Iodine required for synthesis of hormones
What systemic effects do thyroid hormones have on the body:
- Metabolic rate
- Energy requirements
- Oxygen consumption
- Carbohydrate and lipid metabolism
- Growth and development
- Brain functions
Clinical manifestations of hyperthyroidism
- 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
Management of hyperthyroidism
- Antithyroid drugs
- Iodine
- Beta-blockers (symptoms)
- radioactive iodine therapy
- surgical
- nutrition
Hypothyroidism causes:
- autoimmune
- absence of thyroid gland
- lack of TRH related to a tumour or disorder of the hypothalamus
- iodine insufficiency
Clinical manifestations of hypothyroidism:
- 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
Management of hypothyroidism
- thyroid hormone replacement (adjusted according to response, cardiac side effects)
- nutritional therapy
Does the thyroid use positive or negative feedback systems
Negative
Symptoms of hypoglycaemia:
- 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
Function of the pancreas gland:
- 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
Metabolic changes when insufficient insulin is released:
- hyperglycaemia
- glycosuria (glucose in urine)
- polyphagia
- polydipsia
- lipolysis
- ketosis
- acidosis (liver cannot remove all waste products)
Disorders associated with diabetes:
- 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
Clinical signs and symptoms of hyperglycaemia
- fatigue
- lethargy
- irritation
- glycosuria
- polyphagia
- polydipsia
- itchy skin
Signs of impending dangerous complications of hyperglycaemia:
- 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
Metformin (glucophage)
- first line oral med for T2DM
- monitor kidney function
- GI side effects most common
- starting dose matters for tolerability
Three major complications of DM:
- Diabetic ketoacidosis (DKA)
- Hyperosmolar hyperglycaemia state (HHS)
- Hypoglycaemia
What is diabetic ketoacidosis:
- 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
Precipitants of DKA
- 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
Metabolic disturbances in DKA
- Hyperosmolarity
- metabolic acidosis
- extracellular volume depletion
- electrolyte imbalances
Clinical manifestations of DKA:
- 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
DKA investigations:
- 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)
Management of DKA:
- 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
Potassium replacement in DKA:
- 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
Insulin therapy with DKA
- 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
Glucose therapy after DKA
- 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
Other management of DKA
- 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
What is a hyperosmolar hyperglycaemic state (HHS)?
- 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
Causes of hyperosmolar hyperglycaemic state (HHS):
- infection and other acute illnesses, often cardiovascular
- drugs such as beta blockers, calcium channel blockers and diuretics
Patient characteristics of hyperosmolar hyperglycaemia state (HHS):
- patients tend to be older and sicker
- consider pre-existing illness
- higher mortality rate than DKA
Hyperosmolar hyperglycaemic state (HHS) treatment:
- 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
Hyperosmolar hyperglycaemic state (HHS) clinical manifestations:
- 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
Hyperosmolar hyperglycaemic state (HHS) management:
- DRSABCD
- Neurological assessment
- FBE, U&Es/Cr, BGL, blood ketone, ABG
- fluid resuscitation
- electrolyte replacement
- +/- insulin administration
- ECG + cardiac monitoring
- IDC
- septic workup
Causes of hypoglycaemia:
- 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
Acute complications of diabetes:
- hypoglycaemic shock
- hyperglycaemic hyperosmolar state
- diabetic ketoacidosis
Chronic complications of diabetes:
- 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)
HbA1C (glycosylated haemoglobin)
- measures average BGL over 2-3months
- <7% greatly reduces risk of developing microvascular complications
- non-diabetic normal range = 3.5-6%
Glucose excreted in the urine
Glucosuria
Clinical syndrome of hypermetabolism
Thyrotoxicosis
What is the importance of BGL monitoring in the fasting patient
to monitor for hypotension
how frequently should BGL monitoring be performed on the fasting patient
hourly
Clinical manifestations of hyperthyroidism:
- sweating
- startled facial expression
- palpitations
- tachycardia
- flushed skin
- tremor
- hyperexcitable
Clinical manifestations of hypothyroidism:
- coldness
- expressionless face
- weight gain
- personality changes
- hair loss
- hoarse voice
- fatigue
Clinical manifestations of hypoglycaemia?
- confusion
- tachycardia
- drowsiness
- palpitations
- pallor
- sweating
- irritability or anxiety
- slurred speech
hypoglycaemia treatment
- glucose injection
- glucagon injection
- eating/drinking carbohydrates
Clinical manifestations of hyperglycaemia:
- nausea
- acidosis (DKA)
- polyphagia
- polydipsia
- ketosis
- dehydration
- weakness
- polyuria
Main functions of steroid hormone cortisol?
- decrease inflammatory cytokines
- increasing hepatic glucose production
Prolonged use of steroids such as prednisolone may lead to:
Cushing’s syndrome
Hyperosmolar hyperglycaemic state/syndrome (HHS) normally occurs in which type of diabetes
Type 2
What do thyroid hormones impact in the body:
- metabolic rate
- energy requirements
- oxygen consumption
- carbohydrate and lipid metabolism
- growth and development
- brain functions
Inner medulla of the adrenal glands produce which hormones:
- adrenaline and noradrenaline
Outer cortex of adrenal glands produce which hormones:
- corticosteroid hormones (mineralocorticoids, glucocorticoids)
