Disease Flashcards
Hyperthyroidism/thyrotoxicosis
Causes- Excessive stimulation of TSH, autoimmune thyroid stimulation (graves-increase in TSH receptor antibodies due to genetically predisposed defect in immunoregulation), thyroiditis (inflammation of thyroid gland-viral-flu/mumps), toxic multinodular goitre, excessive intake of thyroid meds
Risk factors- genetics, women, increased iodine intake, smoking, stress, postpartum
S&S-
metabolic- wt loss despite increased food intake, heat intolerance, fluid volume deficit, decreased glucose tolerance, increased temp
Cardio- tachycardia, palpitations, HT, arrhythmias
GI- increases bowel movements with diarrhoea, nausea/vomiting, abdo pain
Reproductive- amenorrhea, decreased fertility, increased libido in men, impotence
CNS- irritability, insomnia, hand tremors, nervousness, increased reflexes
Skin- increases sweating, warm and smooth, hair loss, fine hair
Skeletal- increases risk of fractures, muscle wasting, fatigue, weakness, pretibial myxoedema (plaques and nodules on shins-rare)
Resp- dyspnoea
Eyes- exomphthalmos (forward protruding)-graves, proptosis (forward facing eyes)-graves, (these cause blurred vision, dry eyes, inability to close eyelids, photophobia, eye pain)
Endocrine- goitre
Thyroid storm- extreme state hyperthyroid. Caused by infection, stress, trauma, MI, DKA
S&S- hyperthermia, tachycardia, systolic HT, abdo pain, vomiting, diarrhoea, agitation, seizures, delirium
Treat- cooling, fluids, glucose, electrolytes, ventilation, stabilising cardiac function
Diagnosis- TSH (suppressed in graves, not suppressed in pituitary tumour), T3/4 elevated, increased radioactive iodine uptake, thyroid scan, biopsy
Treat- radioactive iodine therapy, antithyroid drugs (carbimazole), propylthiouracil (PTU)- both can cause liver function disturbances and rarely agranulocytosis so needs LFT and to report sore throat and mouth ulcers. surgery
Hypothyroidism
Primary- congenital defects in gland, loss of thyroid tissue (surgery, antithyroid meds, thyroiditis), hashimotos (autoimmune disorders that destroys thyroid tissue)
Secondary- pituitary TSH deficiency or peripheral resistance to thyroid hormones
Reduced intake of iodine (needed to produce TH)- found in food and seafood
S&S
Skin- myxoedema (non-pitting oedema around body), hair loss, brittle nails, coarse dry skin, pallor
CNS- Hans/foot parasthesia, lethargy, somnolence, confusion, decreased reflexes, slow speech, memory impairment
Sensory- periorbital oedema
CVS- hypotension, bradycardia, arrhythmias, cardiomegaly, anaemia
Endocrine- goitre
Resp- pleural effusion
GI- constipation
Muscle- stiffness, weakness, fatigue
Metabolic- decreased appetite, hypothermia, anorexia, wt gain, systemic oedema, elevated serum cholesterol, sleep apnoea
Reproductive- menorrhagia, infertility, decreased libido
Diagnosis- increases TSH and decreased T4
In pregnancy BHCG increases in first trimester and acts like TSH causing mild hyperthyroidism which usually resolves when BHCG declines in second trimester. Antibodies checked as can cross placenta and cause hyperthyroidism in baby. Hypothyroid can cause miscarriage, PTL, poor neurocognitive development
Treat- thyroxine, surgery if goitre affecting breathing
Hyperparathyroidism
Risk factors- age, women
Primary cause- hyperplasia, or adenomas of gland causing unregulated over production of parathyroid hormone- increases absorption of calcium throughout GI tract
Secondary- compensatory response to hyperphosphataemia and hypocalcaemia- increases secretion of parathyroid hormone (found in early kidney disease and Vit D deficiency)
Tertiary- hyperplasia of parathyroid gland and loss of response to serum calcium levels (usually from chronic kidney disease)
S&S-
Muscle- bone pain, pathological fractures, muscle weakness, muscle atrophy
Renal- renal calculi, polyuria, polydipsia
GI- abdo pain, peptic ulcers, pancreatitis, insulin resistance, nausea, constipation
CVS- arrhythmias, HT, deposits of calcium and phosphate in arterial walls
CNS- parasthesia, depression, confusion, psychosis
Metabolic- acidosis, wt loss, fatigue
Diagnosis- rule out other causes of hypercalcaemia, calcium and PTH levels, bone density scan
Treat- IV fluids (prevent dehydration and stones), avoid antacids with calcium/thiazide diuretics/leg doses of Vit A/D. Calcitonin (inhibits bone reabsorption and increases calcium excretion in kidneys), surgery
Hypoparathyroidism
Damage to or removal of parathyroid gland
Unable to reabsorb calcium from bone and regulate calcium absorption in kidneys causing hyperphosphataemia
S&S-
Muscle- spasm, facial grimacing, carpopedal spasms, tetany/convulsions
Skin- brittle nails, hair loss, dry skin, scaly skin
GI- abdo cramps, malabsorption
CVS- arrhythmia
CNS- parasthesia, mood disorder, hyperactive reflexes, psychosis, increased ICP
Diagnosis- low calcium levels, high phosphate in absence of renal failure
Treat- IV calcium gluconate, calcium and Vit D supplements
Hypercortisolism/ Cushing’s
Excessive amounts of circulating cortisol or ACTH
Pituitary form- ACTH hypersecretion by tumour of pituitary
Ectopic form- ACTH secreting tumours (usually of lung or pancreas)
Adrenal form- excessive cortisol secretion by benign or malignant adrenal tumour. Excess secretion suppresses ACTH production resulting in atrophy of uninvolved adrenal cortex
Iatrogenic- long term therapy with pharmological glucocorticoids
S&S-
Metabolic- central obesity, buffalo hump, moon face, altered glucose metabolism may lead to T2DM, hypokalaemia, hypernatraemia
Muscular- peripheral muscle weakness
Skin- ecchymosis, loss of collagen and connective tissue, thinning of skin, abdominal striae, easy bruising, poor wound healing, frequent skin infections
Skeletal- osteoporosis, fractures
CVS- HT (potassium is lost and sodium retained)
GI- increases gastric secretions, peptic ulcers
Renal- renal calculi, polyuria, polydipsia, glycosuria
CNS- depression, psychosis
Reproductive- amenorrhea, hirsutism, acne, menstrual irregularities, infertility, impotence
Diagnosis- plasma cortisol (loss of fluctuations morning/night), plasma ACTH, 24hr urine, serum potassium/calcium/glucose, ACTH suppression test, salivary cortisol levels, MRI, abdo scan
Treat- carbegoline (dopamine receptor agonist), metyrapone (suppresses activity of adrenal cortex and decreases peripheral metabolism of corticosteroids), pasitreotide (binds you ACTH receptors inhibiting secretion), surgery
Hypocorticolism (addisons)
Autoimmune destruction of adrenals
Risk factors- People who are taking anticoagulants, major sepsis, trauma (bilateral adrenal haemorrhage)
Adrenoleukodystrophy- X linked inherited disorder characterised by accumulation of very long fatty acids in the adrenal cortex, brain and spinal cord
ACTH deficit from tumours, surgery, irradiation, use of exogenous steroids
People who have abruptly withdrawn from steroid therapy
Causes a decrease in glucocorticoid and mineralcorticoids which reduces ACTH feedback and ACTH rises
S&S- appears after 90% function lost
Skin- delayed wound healing, hyperpigmentation, loss body hair, dehydration
CVS- postural hypotension, arrhythmia, tachycardia, anaemia
CNS- lethargy, tremors, emotional lability, confusion
Muscle- weakness, wasting, joint pain, muscle pain
GI- anorexia, nausea/vomiting, diarrhoea
Reproductive- menstrual changes
Metabolic-hyperkalaemia, hyponatraemia, hypoglycaemia, malaise, wt loss
Addisons crisis- high fever, weakness, severe penetrating pain in abdo, lower back pain, severe vomiting, diarrhoea, hypotension, circular collapse, shock, seizures, coma
Diagnosis- serum cortisol, BGL, serum sodium, serum potassium, BUN, plasma ACTH, CT scan
Treat- hydrocortison, mineral corticoids
Anterior pituitary
Hypersecretion PRL=irregular menses, infertility, impotence, decreased libido
Excess GH=gigantism
Deficient GH= acromegaly- usually from tumour (enlarged extremities, enlarged forehead, tongue enlarged, voice deepens, pins and needles in hands, joint pain, headache, barrel chest, gap in teeth, thick/oily skin, strong body odour, hair overgrowth, heavy sweating, HT, congestive heart failure, impaired glucose tolerance)
Syndrome of inappropriate ADH
High levels of ADH in the absence of serum hypoosmalality
Caused by ectopic production from malignant tumours, transient form with head injury, pituitary surgery, or meds (barbiturates, anaesthetic, diuretics)
ADH release continually and acts on renal tubules and collecting ducts increasing water reabsorption. Decrease in sodium concentration affects neuron function.
Blood volume expands but plasma volume diluted, aldosterone suppressed which leads to increased renal excretion of sodium, water moves into cells from interstitial space
S&S- brain cells swell= headache, changes in personality, lethargy, irritability, wt gain (retention of fluid), no oedema as fluid distributed between intra/extracellular spaces
Diagnose- low serum osmolarity/hyponatraemia, urine hyperosmolarity, urine sodium excretion that matches intake, normal adrenal and thyroid function, absence of conditions that can alter fluids status
Serum electrolytes, serum osmolarity, urine volume, urine electrolytes, urine osmolarity, chest X-ray (to rule out resp condition)
Treat- IV hypertonic fluid, fluid restriction <800mls day, demeclocycline (antibiotic that produces excessive urine flow)
Diabetes insipidus
ADH insufficiency
Neurogenic- abscence of ADH due to damage/inflammation/disruption of hypothalamus and pituitary gland, or idiopathic
Nephrogenic- renal tubules are not sensitive to ADH (congenital or renal failure) occurs with disease that damage renal tubules (pyelonephritis/drugs)
S&;S- polyuria, extreme thirst-polydipsia, dehydration, hypernatraemia, low urine specific gravity, nocturia, low urine osmolarity
Diagnose- clinical symptoms with urine and serum osmolarity and serum sodium following water deprivation
Treat/ IV hypotonic fluids, increasing oral fluids, replace ADH
T1DM
Characterised by hyperglycaemia, breakdown of body fats and proteins, development of ketosis
Risk factors- genetics (DR3 and DR4 antigens on chromosome 6), environmental factors (viral infections, chemical toxins)
Results from destruction of beta cells of islet of langerhans
Autoimmune or idiopathic
Autoimmune destruction of islet cells. Slowly destroys beta cell production of insulin with onset of hyperglycaemia after 80-90% destruction.
Hyperglycaemia causes serum hyperosmolarity drawing water from intracellular spaces in circulation. Increased blood volume increases renal blood flow and results in polyuria, glucosuria, decrease in intracellular volume causes dehydration=thirst/polydipsia.
Energy production reduced due to glucose not being able to get into cells which stimulates hunger and eating more (polyphagia), wt loss due to water loss and breakdown of fat/protein for energy, blurred vision from osmotic effects causing swelling on lens of eye
Diagnosis- random BGL >11.1, fasting >7.0, OGTT 2hr >11.1
Impaired glucose if OGTT at 2hrs is 7.8-11.0 or fasting 6.1-6.9
HBA1C (average BGL over 2-3months as excess glucose binds to haemoglobin) <7%, urine glucose levels (glucouria indicates hyperglycaemia, ketones indicate diabetic keto acidosis), urine albumin (can indicate nephropathy), serum cholesterol, serum electrolytes, BGL fingerprick (if haematocrit low then BSL will be falsely high and vice verse)
Treat- insulin’s (derived from pork pancreas or synthesised)
Ultra short acting - onset 5-10mins, duration 5 hours, eat immediately after injecting (novorapid, humalog)
Short acting- onset 30mins, duration 8hours (actirapid, humulin R)
Intermediate- cloudy, upturn to mix first, onset 1.5hrs, duration 12-24hrs (protophane, humulin NPH)
Long acting- no peak action, last 24Hrs (levemir, lantus)
Mixed- short/fast with intermediate 30/70 or 50/50, cloudy, upturn to mix first (humulog mix, novomix, mixtard)
Oral hypoglycaemics- metformin, sulfonylurea
Nutrition- low GI carbs, soluble fibre (reduces blood glucose and cholesterol, reduced sugar and trans/saturated fats
Complications- DKA, HHS
Neurological- somatic neuropathies-(parasthesia, loss of cutaneous sensation, loss of fine motor control), visceral neuropathies- (sweating disfunction, pupillary constriction, fixed heart rate, constipation, diarrhoea, incomplete bladder emptying, sexual dysfunction)
Sensory- diabetic retinopathy, cataracts, glaucoma
CNS- orthostatic hypotension, accelerated atherosclerosis, cerebrovascular disease (stroke), coronary artery disease (MI), peripheral vascular disease, blood viscosity, platelet disorders, left ventricle hypertrophy
Renal- HT, albuminuria, oedema, chronic renal failure
Muscle- joint contractures
Skin- foot ulcers, gangrene, atrophic changes
Immune- impaired healing, chronic skin infections, periodontal disease, UTI, lung infections, vaginitis
T2DM
Fasting hyperglycaemia despite availability of insulin
Cellular resistance to effects of insulin.
Resistance is increased by obesity, inactivity, illness, medications and ageing
Risk factors- family hx, obesity, physical inactivity, race/ethnicity, women-PCOS/GDM, HT, metabolic syndrome
S&S- polyuria, polydipsia
, blurred vision, fatigue, parasthesia, skin infections, keto acidosis (increased metabolism of fats/protein), tachypnoea (increased ketones=acidosis, resp system increases to buffer acidosis and blow off keytones leads to acetone breath)
Dawn effect- high fasting BGL due to nocturnal elevation of GH that decreases metabolism of glucose by muscle and fat
Diagnosis- random BGL >11.1, fasting >7.0, OGTT 2hr >11.1
Impaired glucose if OGTT at 2hrs is 7.8-11.0 or fasting 6.1-6.9
HBA1C (average BGL over 2-3months as excess glucose binds to haemoglobin) <7%, urine glucose levels (glucouria indicates hyperglycaemia, ketones indicate diabetic keto acidosis), urine albumin (can indicate nephropathy), serum cholesterol, serum electrolytes, BGL fingerprick (if haematocrit low then BSL will be falsely high and vice verse)
Treat- insulin’s (derived from pork pancreas or synthesised)
Ultra short acting - onset 5-10mins, duration 5 hours, eat immediately after injecting (novorapid, humalog)
Short acting- onset 30mins, duration 8hours (actirapid, humulin R)
Intermediate- cloudy, upturn to mix first, onset 1.5hrs, duration 12-24hrs (protophane, humulin NPH)
Long acting- no peak action, last 24Hrs (levemir, lantus)
Mixed- short/fast with intermediate 30/70 or 50/50, cloudy, upturn to mix first (humulog mix, novomix, mixtard)
Oral hypoglycaemics- metformin (increase glucose uptake and usage at target tissues.
sulfonylurea (act on pancreatic beta cells to increase secretion of insulin).
Acarbose (slow digestion and absorption of carbohydrates from digestive system and slowing rise in BGL)
Nutrition- low GI carbs, soluble fibre (reduces blood glucose and cholesterol, reduced sugar and trans/saturated fats
Complications-
Cardiovascular- thickening of basement membrane and endothelial hyperplasia. Molecules with glucose attached are deposited in walls of blood vessels. Dyslipidaemia, MI, HT, congestive heart failure, stroke
Retinopathy- stage 1 -
Nonproliferation- increase retinal capillary permeability, vein dilation, micro aneurysm
Stage2- pre proliferation- progression of Ischaemia with areas of poor perfusion that culminate in infarcts
Stage3- proliferative- results of neovascularisation and fibrous tissue formation within retina
Kidneys- renal failure- glomeruli damaged by high systemic flow and protein denaturation as high glucose levels change protein shape. Microalbuminuria (small amounts albumin in urine) first sign and reduction in insulin requirement
Neuropathy- neurons don’t need insulin for glucose to enter cells so increased glucose enters neurons and cause degeneration and delay in conduction
Infection- due to impair sensation (pain/touch) decreases bodies natural protection reflexes
Hypoxia-glycated haemoglobin impedes O2 release reducing skin integrity
Pathogens proliferate rapidly in high glucose content
Blood supply- decreases due to vascular changes and reduces WCC to reduce infection
WCC function impaired
Amputation/ gangrene/ ulcers
Diabetes in older adults
S&S- orthostatic hypotension, periodontal disease, infections, stroke, gastric hypotony, impotence, neuropathy, confusion, lethargy, leg cramps, gradual wt gain, glaucoma
Diabetic keto acidosis
Release of free fatty acids which leads to loss of bicarb and metabolic acidosis, hyperosmolarity from hyperglycaemia and dehydration, extracellular volume depletion from osmotic diuresis, electrolyte imbalances- suppresses CNS and can lead to coma
Due to stress/infection and release of GH, adrenaline and cortisone
Deficiency in insulin causes fat breakdown to create energy instead of glucose and causes ketone release, high glucose draws water out of cells and into urine leading to polyuria/glucosuria and dehydration
S&S- flushed warm skin, thirst, fruity breath, decreased BP, tachycardia, kussamauls resps, confused, nausea/vomiting, altered consciousness, wt loss, weakness, moderate fluid loss, dehydration, abdo pain
Bloods- glucose >16, keytones increased, potassium/sodium/chloride abnormal, pH <7.3, osmolality >340
Treat- insulin, fluids, electrolytes, ABC
Hyperosmolar hyperglycaemic state (HHS)
Plasma osmolarity of 340mmol/kg or greater and glucose over 33. Life threatening situation
Large amount of glucose through kidneys leads to hypovolaemia and hypotension, osmolality of blood becomes high. Sufficient insulin so fat does not break down and create keytones
S&S- flushed warm skin, thirst, normal breath, decreased BP, tachycardia, lethargic, nausea/vomiting, profound fluid loss, altered consciousness, weak, wt loss, malaise, seizures
Bloods- glucose >33, ketones normal, potassium/sodium/chloride abnormal, normal Ph, osmolality >340
Treat- insulin, IV fluids, electrolytes
Hypoglycaemia
BGL 2.5-3.3
S&S- hunger, sweating, pallor, shakiness, irritability, anxiety, nausea, tachycardia, cool skin, hypotension, slurred speech, headache, blurred vision, decreased consciouness, seizures, difficulty thinking
