Endocrine Flashcards
what is the relationship between hypothalamus, pituitary and adrenal gland
hypothalamus releases releasing hormones to pituitary in brain
pituitary releases secreting hormones to adrenal
adrenal gland feeds back to hypothalamus
what things can go wrong with glands (3)
overproduction
underproduction
benign/malignancy
where do we find adrenal glands
1 on the superior aspect of each kidney
what is the shape and structure of an adrenal gland
triangular/pyramidal in shape
Composed of cortex and medulla.
Cortex (outer part) composed of three layers; zona glomeruloa (produces aldosternone), zona fasciculata (produce cortisol), zona reticularis (produce androgenic steroids).
Medulla (inner part of gland) produces stress hormones (adrenaline and noradrenaline).
what is the cortex of the adrenal gland split into and what do they produce
Cortex (outer part) composed of three layers; zona glomeruloa (produces aldosternone), zona fasciculata (produce cortisol), zona reticularis (produce androgenic steroids).
what does the medulla of the adrenal gland produce
produces stress hormones (adrenaline and noradrenaline).
how can we detect adrenal problems
24 hour cortisol urine test
Serum ACTH levels
Diurnal pattern of serum cortisol levels
Dexamathasone suppression test
what are the 3 main pathway causes of adrenal problems
Secondary: disease of pituitary or hypothalamus
Primary: adrenal disease: Developmental, haemorrhagic necrosis, autoimmunity, destruction by TB or tumour
Iatrogenic: Suppression due to steroid therapy
if the adrenal gland is yellow and cheese like in the middle, what is the likely cause
tuberculosis
what does Waterhouse-Friderichsen syndrome affect and how does it resent
causes haemorrhage of the adrenal gland cortex
adrenal glands turn black with blood clot
what are some effects of adrenal insufficiency
Skin pigmentation
Hypotension
Muscle weakness
Hypoglycaemia
Hyponatraemia
Hyperkalaemia
Renal dysfunction
what are some causes of adrenal overactivity
Cushing’s syndrome - adrenal tumours, iatrogenic
Cushing’s disease – pituitary microadenomas
Conn’s syndrome - excessive aldosterone
compare cushing’s syndrome and cushings disease
Cushing’s syndrome - adrenal tumours, iatrogenic
Cushing’s disease – pituitary microadenomas
what does Cushing’s syndrome cause
Obesity
Hypertension
Osteoporosis
Hyperglycaemia
Myopathy
Skin atrophy
Polycythaemia
Susceptibility to infection
what is Paroxysmal hypertension and what is this a key sign of
rapid increase in blood pressure that slightly decreases over time
sign of Phaeochromocytoma
what is Phaeochromocytoma and what is its key symptom
Tumour adrenal medulla forming a catecholamine producing tumour
Paroxysmal hypertension
how do we decide the behaviour of pheochromocytoma
PASS: pheochromocytoma of adrenal gland scoring system.
Could be malignant or benign. Metastasis is indicator of malignancy.
what is the pathway of thyroid gland secretions
hypothalamus secretes thyroid releasing hormone TRH
pituitary released thyroid stimulating hormone TSH
thyroid releases T3 and T4 - inhibit hypothalamus and pituitary
how might we diagnose thyroid problems
Serum T3, T4, TSH, calcitonin
Ultrasound
Radioactive iodine uptake studies
FNA cytology - fine needle aspiration
Core biopsy
why is cytology good for thyroid diagnosis and why might it be disadvantageous
Safe- Reduces need to excise benign lesions
Thy 1-5 categories
Can establish diagnosis of some types carcinoma: papillary, medullary, anaplastic
Can’t distinguish between benign and malignant follicular lesions
which type of thyroid cancer can cytology not differentiate between malignant and benign
follicular
what might cause hypothyroidism
Iodine deficiency
Developmental
Autoimmune
Radiotherapy, radioiodine therapy
Drugs
what might cause hyperthyroidism
Autoimmune
Toxic adenomas
masses
what is goitre
swollen thyroid gland = large swollen neck
name the 2 most common autoimmune thyroid disorders
Hashimoto thyroiditis
Graves disease
what is hashimoto thyroiditis and who is likely to get this and what does it present as
Middle aged, women
Auto-antibodies against Thyroglobulin and Thyroid peroxidase
Lymphocyte mediated destruction of thyroid follicles
how would hashimoto thyroiditis present clinically and histologically
Initial hyperthyroidism followed by hypothyroidism
Painless enlarged thyroid
histologically Lymphocyte mediated destruction of thyroid follicles
how do we treat hashimoto thyroiditis
life long thyroxine
what 2 risks are there from having hashimoto thyroiditis
Risk of developing other autoimmune disease
Low Risk for thyroid malignancy
what is Graves disease
most common cause of hyperthyroidism
Production of Thyroid stimulating immunoglobulin
Anti-TSH receptor antibodies
Diffuse process histologically affecting all of the lobe and both lobes
can lead to cellulitis
how would a Graves disease blood test present
Elevated T3 and T4. Low TSH
Increased uniform radio-iodine uptake
how do we treat graves disease (3)
Treated with anti-thyroid medications
radio-iodine ablation
surgery
what is the most common benign neoplasm of the thyroid gland
Follicular adenoma
usually solitary encapsulated
what is the most common malignancy in thyroid tissue
papillary carcinoma 60-70% of cases
in young adults
lymphatic spread - good prognosis usually
what is the prognosis of papillary carcinoma of the thyroid and why
usually good
metastasises via lymph nodes, not blood
how would papillary/follicular carcinomas look histologically
optically clear nuclei ‘orphan annies eyes’
overlapping nuclei
overcrowding
if thyroid tissue has clear overcrowded nuclei, what is the likely diagnosis
papillary carcinoma
compare follicular and papillary carcinomas of thyroid
papillary : 60-70% of carcinomas, young adults, good prognosis, lymph spread
follicular: 20-25%, young-middle age, blood stream, worse prognosis
how might we know if a thyroid cancer is malignant histologically
clear nucelli - papillary carcinoma
vascular invasion into the blood vessel
capsular invasion
what is the least common thyroid carcinoma
medullary 5-10%
elderly but familar cases earlier in life
lymphatic and blood stream spread
variable prognosis
thyroid cancer has spindle cell morphology, what type of carcinoma is this?
medullary
calcitonin histocytochemistry can be used to diagnose what and how would it show and what else would give this stain
medullary carcinoma
stain tissues brown
C cell hyperplasia
what type of cell does medullary carcinoma affect
C cells
if a thyroid cancer has nests of cells, signs of necrosis and increased mitosis what ttype of carcinoma is this
poorly differentiated carcinoma
why is anaplastic carcinoma very low prognosis
it has very aggressive local spread
what is anaplastic thyroid carcinoma
occurs in elderly with very agressive local spread = very poor prognosis
very varied cells and nuclei
what is the commonest cause of thyroid lymphoma
hashimotos thyroiditis
what does insulin do
convert glucose to glycogen = reduced glucose blood levels
what does glucagon do
convert glycogen to glucose
increase glucose blood concentrations
in the fasting state, where do w get glucose from (2)
mainly the liver, sometimes the kidney
what percent of glucose goes to muscle and liver after eating
40% goes to the liver
60% goes to muscle
if glucose and glycogen is low in fasting state, what do we use for energy
lipids and FFA free fatty acids
beta oxidation
forms ketone bodies as a side product
what part of the pancreas produces glucagon and insulin (3)
endocrine section of pancreas
islets of langerhans
beta cells = insulin
alpha cells = glucagon
explain the paracrine hypothesis with glucose homeostasis
this explains crosstalk between beta and alpha cells
high insulin levels keep alpha cells inhibited
when insulin drops (due to low glucose), alpha cells are no longer inhibited
therefor produce glucagon
what does glucose pass through to enter a beta cell of the pancreases
GLUT2 receptor
explain glucose action on a beta cell (how this leads to insulin release)
glucose enters cell via GLUT2 channel
reaction occurs glucose (glucose kinase) –> ATP/ADP
this closes potassium channel = depolarized cell membrane
calcium channels open and calcium enters
Calcium triggers insulin release
explain how insulin acts on a fat/muscle cell
insulin attaches to insulin receptor
cascade of reactions activating intracellular GLUT4 vesicles
mobile GLUT4 vesicles integrate to plasma membrane
allows glucose to enter the cell
explain how insulin acts on a fat/muscle cell
insulin attaches to insulin receptor
cascade of reactions activating intracellular GLUT4 vesicles
mobile GLUT4 vesicles integrate to plasma membrane
allows glucose to enter the cell
what is the name of the vesicle that insulin acts on
intracellular GLUT4 vesicle
give the 3 major affects of insulin
supresses hepatic glucose output e.g. gluconeogenesis and glycogenolysis
increase glucose uptake by insulin sensative cells e.g. fat and muscle
supresses lipolysis and muscle breakdown
what is a counterregulatory hormone and give examples
hormones that oppose the action of insulin
glucagon
also adrenaline, cortisol, growth hormone
what is the action of counterregulatory hormones (3)
opposite of insulin
1. increases hepatic glucose output e.g. gluconeogenesis and glycogenolysis
2. decreases glucose uptake in sensitive cells e.g. fat and muscle
3. stimulate peripheral release of glucose, FFAs and muscle breakdown
what is the risk of a diabetic having high adrenaline
adrenaline is a counterregulatory hormone, opposing insulin action
what are symptoms of HYPOglycemia
sweating
feeling tired
dizziness
feeling hungry
tingling lips
feeling shaky or trembling
a fast or pounding heartbeat (palpitations)
becoming easily irritated, tearful, anxious or moody
turning pale
what are symptoms of hyperglycaemia
feeling very thirsty
peeing a lot
feeling weak or tired
blurred vision
losing weight
what is diabetes mellitus
disorder of carbohydrate metabolism and homeostasis leading to hyperglycaemia
what can acute hyperglycaemia cause (2)
diabetic ketoacidosis DKA
hyperosmolar hyperglycaemic state = coma
what can chronic hyperglycaemia cause
tissue complications with vessels e.g. blood vessels in heart, brain, periphery, legs
limbs = amputation
brain = stroke
heart = heart failure
mouth = bleeding and periodontitis
what are the 3 types of problems that come with diabetes
acute hyperglycaemia = diabetic ketoacidosis (DKA) and hyperosmolar coma (Hyperosmolar Hyperglycaemic State )
chronic hyperglycaemia = tissue complications = stroke, leg arteries = amputation
medication related hypoglycaemia
what oral symptoms of diabetes are there (4)
slow wound healing in the mouth
halitosis = ketone bodies
increased periodontitis and BOP
oral candidiasis = reduced fungal response
a patient has oral candidiasis and slow healing wounds in the mouth. What could they have
undiagnosed diabetes
what types of diabetes are there (5)
type 1
type 2 (including gestational)
MODY - Maturity onset diabetes of youth (MODY), also called monogenic diabetes
pancreatic diabetes
“Endocrine Diabetes” (Acromegaly/Cushings)
what is pancreatic diabetes
where there is uncontrolled glucose homeostasis due to an insult to the pancreas
possibly trauma or surgery or cancer altering the function of the pancreases
what is MODY
Maturity onset diabetes of youth (MODY), also called monogenic diabetes
diabetes caused by a genetic factor
why does uncontrolled diabetes lead to thirst
the kidney usually reabsorbs all glucose back into the blood
can only absorb 11mol/L
over this amount, glucose stays in the collecting duct
glucose acts as an osmotic agent pulling more fluid into the collecting duct, increasing volume of urine
body looses more fluid, therefor pt gets more thirsty
how much glucose can a healthy kidney reabsorb
11mol/L
how long do red blood cells stay in the body and where do they get destroyed after this time
remain in the blood stream for 120 days
then get decommissioned in the spleen
what is the HbA1c level and why is this significant
amount of glycated haemoglobin
above 48mmol/mol or 6.5% = diabetic
why do we have to be careful using HbA1c levels for diabetes detection (2)
any problem that alters RBC presence or destruction e.g. splenomegaly or acute blood loss = false negative
iron deficiency anaemia can make RBC last longer and give false positives
how does iron deficient anaemia affect HbA1c levels
this leads to RBC lasting longer in the blood stream
gives higher levels of HbA1c = false positive diabetes
what diagnostic values are there for positive diabetes
random blood glucose levels > 11mmol/L
fasting plasma glucose levels > 7mmol/L repeated 2 times
HbA1c levels > 48mmol/mol 6.5%
what is the type I diabetes
autoimmune disease where a cross reaction leads to antibodies that attack beta cells of the islets of Langerhans possibly due to a virus
no beta cells
no insulin production
why does type I diabetes lead to hyperglycaemia (3)
no insulin therefor:
-glucagon levels remain high
-no glucose uptake in insulin sensitive cells
-hepatic breakdown of glycogen and fats
what would be the cause of death in a type I diabetic uncontrolled state
diabetic ketoacidosis
explain why diabetic ketoacidosis is dangerous and how it comes about
occurs as body needs fuel but cannot use glucose as it is all in the vessels
uses fat beta oxidation for fuel
side product is ketones
ketones as slightly acidic and builds up in the blood = poison
causes vomiting, passing a lot of water, hyperventilating to remove acidic CO2
leads to dehydration and kidney failure
what is the bodies reaction to diabetic ketoacidosis (4)
vomiting due to blood poisoning
polyuria and polydypsia
hyperventilation to remove acidic CO2
loose weight as we are loosing glucose (urine) and fat (beta oxidation)
what two factors lead to impaired insulin tolerance in type II diabetes
impaired insulin secretion (genetic)
acquired insulin resistance (environmental)
why does insulin resistance occur
increased weight = increased fat = larger cells and change in morphology of the cells and receptors = insulin resistance
why might a type II diabetic be on insulin injections
after about 10 years body declines in insulin sensitivity
may be complete insulin resistant
do macrovascular or microvascular problems come first in pre-diabetes
macro come first
how many grams of sugar do we give to test the pancreas for diabetes
75 grams
what is treatment for hypoglycaemia
how do we treat type II diabetes
exercise and weight loss
controlled diet
control blood pressure and other symptoms
possibly insulin shots if progressive type II diabetes = insulin resistance
what is gliclazide mainly used for
treatment of type 2 diabetes
type of sulphnylureas that keeps potassium ion channel shut = release of insulin
what must we ensure a patient does before a dental procedure if they are on gliclazide and why
eats breakfast before
glyclazide is a sulphonylureas and increases insluin
if not eationg = hypoglycaemic attack
what are Sulphonylureas and give the main type of this drug
drug used for type 2 diabetes top increase insulin secretion
gliclazide
how do sulphonylureases work
close K+ channels on beta cells in pancreas
causes depolaization by Ca2+ and insulin release
type 2 diabetes
what 2 risks come with medication for type II diabetes
weight gain
hypoglycaemia
what are DZTs used for
type II diabetes
what 6 types of medication might a type II diabetic be on
first line
Metformin
second line
DZTs
GLP-1 analogues
DPP-Iv inhibitors (stop break down of GLP-1)
SGLT2
replacing sulphonyureases e.g. gliclazide
what are the affects of GLP-1 analogues
stimulate insulin secretion
reduce apatite
slow gastric emptying
improve insulin sensitivity
where is GLP-1 secreted and what is its function and how do we use this theraputically
L cells in the duodenum
causes slower gastric emptying, reduces apatite, increases insulin sensitivity and production
to make us feel full and not eat any more
GLP-1 analogue drugs used in type II diabetes
how do DPP-IV inhibitors work (4)
DPP-IV is an enzyme that breaks down GLP-1
GLP-1 is secreted by L cells of the duodenum
GLP-1 causes insulin sensitivity, decreased gastric emptying, decreased hunger, insulin release, glucagon inhibition
type II diabetes
what type of drug are vidagliptin and sagliptin
DPP-IV inhibitors
suffix ‘gliptin’
prevent breakdown of GLP-1 for type II diabetes
what is gliptin the suffix for
medications of the class DPP-Iv inhibitors for type II diabetes
prevent breakdown of GLP-1
what medication other than insulin can be used in type I and II diabetes
SGLT2
prevent reabsorption of glucose in the kidney
what is the main side effect of SGLT-2
genital thrush
how do SGLT2 work
prevent reabosprtion of glucose in the kidney
what is astrflozin, glutaflozin and canagliflozin
SGLT2 drugs
prevent reabsorption of glucose in the kidney
what is the suffix ‘ flozin ‘ for
SGLT2 diabetes medication
prevent reabsoprtion of glucose in the kidney
what is the first line drug for type II diabetes
metformin
how does metformin work
reduce production of glucose by the liver
decrease absorption of glucose by the gastrointestinal tract
and increase target cell insulin sensitivity
other than fingerpick monitoring, how else can we monitor blood glucose
continuous glucose monitoring device e.g. libre
what is a limitation of continuous blood glucose monitoring devices
they test the interstitial fluid glucose levels which might not represent blood glucose levels in real time
how do we treat hypoglycaemic attack
20g of rapidly acting carbohydrate e.g. glucose syrup
slow release carbohydrate afterwards to manage
what hormones does thyroid gland produce with their roles
thyroxine T4
T3 tri-iodotryonine
both control basal metabolic rate
calcitonin - regulates calcium levels in the blood
what is unique about the thyroid gland
stores high amounts of inactive hormone in extracellular follicles
also largest endocrine gland in body
what happens if a healthy individual goes into hypoglycaemia and how does this change in diabetes
glucagon, cortisol and adrenaline (counterregulatory hormones) released
in diabetes, if the pt has many hypo attacks, their resistance to it dampens and they may not have the same respsonse
meaning when in hypo, they may not show common adrenaline symptoms e.g. sweating
so hypo may be more difficult to spot
compare primary and secondary hypothyroidism
primary = thyroid underproducing T4 and T3
secondary = pituitary or another factor leading to less TSH and therefor less T3 and T4
what aspects of the type of hypothyroidism affect goitre
T3 and T4 dont make a difference
if TSH is increased, this is driving the thyroid to produce more = enlarged thyroid gland = goitre
what type of hypothyroidism doesn’t lead to goitre
secondary hypothyroidism as no TSH to drive hyperplasia
what are some major symptoms of hypothyroidism
tiredness and increased sleep
mennorhagia
macroglossia
cold intolerance
central swelling (large stomach and breast)
dry skin
weight gain
what are some facial features of hypothyroidism
macroglossia
periorbital oedema
delayed eruption
enamel hypoplasia
thick lips
facial puffiness
causes of primary hypothyroidism (4)
autoimmunity - hoshimotos thyroiditis
iodine deficiency
post radioactive iodine for hyperthyroidism
thyridectomy
causes of secondary hypothyroidism (3)
pituitary tumours
pituitary granulomas
empty sella
give indications for thyroid screening
past radiation
symptoms
congenital hypothyroidism
what is the main cause for hyperthryoidism
autoimmune disease
e.g. graves disease
what are common symptoms of hyperthyroidism
heat intolerance
palpitations
anxiety and irritability
weight loss
loose bowels
tachycardia
warm moist skin
what might lead us to try and diagnose graves disease
hyperthyroidism signs and symptoms
history of other autoimmune disease
diffuse goitre
bulging eye signs oedema
red shins
what are the eye signs of graves disease
eye lids retracted
can see the sclera above the iris
dryness of eyes
bulging eye
how do we treat hyperthyroidism
anti-thyroid medication for 12 months
stop treatment, 50% will never get hyperthyroidism again, 50% will
if they do, surgery or raidoactive iodine (sometimes straight to this)
what are some dental signs of hyperthyroidism
accelerated eruption
mx/mn osteoperosis
increased suseptability to caries and periodontal disease
what are some dental considerations for hyperthyroidism
Increased susceptibility to caries
Periodontal disease
Increased sensitivity to epinephrine which may result in arrhythmias or palpitations
Surgery, oral infection and stress may precipitate thyroid crises
if we see a thyroid nodule what do we do
ask about onset
history of nodule
record size
refer for ultrasound
what special test would we do for a thyroid nodule
ultrasound
thyroid level tests
if NOT hyperthyroid, give FNA
why would we not FNA a patient who is hyperthyroid
push them into hyperthyroid crisis
why would we FNA a thyroid nodule
if they are not hyperthyroid and they have an abnormal ultrasound
Fine needle aspiration gives us a histological diagnosis to see if the nodule is benign or malignant
what does the anterior pituitary gland produce with their peripheral actions (4)
LH and FSH –> oestrogen and androgen
GH –> IGF-1
TSH –> T3 and T4
ACTH –> cortisol
what does the posterior pituitary gland gland
produced in hypothalamus, stored in pituitary
Vasopressin ADH - water absorption
oxytocin- uterine contractions and milk
what (types) symptoms of pituitary dysfunction (3)
hormone excess - too much cortisol = cushings or acromegaly
mass excess = headache, double vision, loss of peripheral vision
hormone deficency = lack of growth, lack of cortisol, hypothyroid
what special investigation do we do if we suspect pituitary problems
MRI
what hormonal symptoms might indicate pituitary problems
low sperm count/infertility/loss of erections/loss of period
hypothyroidism
short growth and lack of energy
adrenal failure
diabetes incipidus
what is ADH used for
water reabsorption in the kidneys
what is diabetes insipidus and its cause
lack of ADH
lack of reabsorption in the kidneys
polyuria and polydipsia
what is sheehans syndrome
post pregnancy if mother lost a lot of blood
leads to infarct in pituitary
hypopituitary
what causes hypopituitary
damage
radiotherapy
infarction
trauma
tumour
infection e.g. TB and syphilis
Sheehan syndrome (post pregnancy)
after head injury, the patient starts urinating a lot and isnt recovering
what might be the cause
pituitary trauma
lack of ADH and cortisol
how do we test for acromegaly
IGF levels and then MRI of pituitary
after surgery how can we treat acromegaly
radiotherapy and medications such as somatostatin (acts against growth hormone)
pt on somatostatin, what does this treat
NOT HIGH BP
inhibits IGF-1 treats acromegaly
pt has widening teeth spaces and sleep apnoea, what could be the cause
acromegaly
what happens to cortisol throughout the day and why is this important to know
highest peak at 1 hour after waking
gradually go down to sleep
low overnight
take into account when testing cortisol levels
what is cushing’s syndrome
where adrenal gland produces too much cortisol
what are some causes of cushings syndrome (4)
pituitary tumour 70-80%
adrenal tumour 10-20%
eptopic tumour e.g. lunch 10%
MOST COMMON iatrogenic = steroids from medications
what are symptoms of cushings syndrome
weight gain
moon face - bull neck
bruising
‘buffalo hump’
acne
stretch marks
diabetes
how do we test for Cushing’s syndrome
give pt a steroid the night before
healthy pt = steroid levels go down
cushings = pt keeps producing steroid
if we get a positive steroid supression test, what is the next step
MRI of pituitary or CT of adrenal glands
pt has central obesity and purple strecth marks. what is the cause of this
cushings syndrome
what is the name for primary adrenal insufficency
addisons disease
what type of disease is addisons disease
primary adrenal insufficiency
why do patients with addisons disease get pigmentation
Addison’s disease is adrenal insufficiency
pituitary gland produces Melanocyte stimulating hormone MSH
if cortisol is reduced, the pituitary gland is not inhibited so produces more ACTH and more melanocyte stimulating hormone MSH
leads to dark pigmentation of the skin
pt has dark pigmentations in their mouth, what is this
addisons disease
primary adrenal insufficiency
lack of cortisol = lack of pituitary inhibition = more release ofLMSH melanocyte stimulating hormone
what is secondary adrenal insufficiency
where pituitary gland doesnt produce any ACTH so reduced cortisol
what are primary causes of primary adrenal insufficency
autoimmune
tubercerlosis
fungal infection
congenital adrenal hypoplasia
what are the causes of secondary adrenal insufficency
medication of steroids!!! if pt on steroids for long time have reduced reliancy on adrenal gland so if they go into a stressful situation or infection, they need more steroids to prevent adrenal crisis
tumour in pituitary or hypothalamus
a patient is on predisolone for 10 years and has an abscess. how do we treat, non surgically?
antibiotics e.g. metronidazole
AND STEROIDS as infection means stress and secondary adrenal insiufficency
if no added steroids, patient will go into adrenal crisis
what is the death rate of adrenal crisis
6-8%
what percent of the population is on steroids and have adrenal insufficency
3% on steroids
50% of them have adrenal insufficency
what are signs of adrenal insufficency
weakness
loss of weight
vomiting
hypotension
salt craving
hypoglycaemic episodes
IF PRIMARY = skin pigmentation
how do we investigate adrenal insufficiency
inject with ACTH
test for cortisol spike
if a pt is on steroids, what steroid precautions must we take for a minor procedure
if high enough e.g. >7mg prednisolone
double dose one hour before surgery
double dose for 24 hours after surgery
if a pt is on steroids, what steroid precautions must we take for a major procedure (GA)
100mg IM of hydrocortisone before procedure
double oral dose for 24 hours after
what 4 main endocrine problems must we understand and treat before dental surgery and why
adrenal suppression : double oral dose or give 100mg hydrocortisone IM
hyperthyroidism: must slow down thyroid before or = thyroid crisis
Cushing’s syndrome: high steroid = avoid infections and pathological fracture so control
Phaechromocytoma: adrenal gland too much adrenaline, if not treated this can cause excess adrenaline and cardiac arrest
what are endocrine causes of hypertension (4)
primary aldosteronism = renal gland = too much aldosterone
pheochromocytoma = too much adrenaline
acromegaly = too much GH
cushings syndrome = secreting excess steroids
hyperthyroidism (not strong relationship)
what is calcium important for (4)
coagulation factors
nervous function
skeletal mineralization
membrane polarization e.g. muscle contraction, release of insulin
what is the function of PTH (1) and how does it act (3)
to increase calcium in the blood
increase bone resorption
increase calcium re-absoprtion and reduces phosphate re-absorption in kidney
increase calcium absorption in intestine (by activating vitamin D)
what are some causes of hypocalcaemia (4)
post surgery/radiotherapy
inherited autosomal dominant hypocalcaemia
syndromes e.g. Di George
chronic renal failure (kidney needed for vitamin D activation)
acute pancreatisis
magnesium deficiency - mg needed to stimulate pth release
pseudohypothyroidism
why does renal failure cause hypocalcaemia
kidney is site of vitamin D activation
Vitamin D upregulates calcium absoprtion
what are the affects of low Mg levels in the blood
hypocalcaemia
need magnesium to stimulate PTH release
low PTA = low calcium
what is pseudoparathyroidism
where we produce PTH however the tissues that accept PTH are less sensative to PTH = low calcium
if someone has multiple blood transfusions, what might they acquire
hypocalcaemia
what are the symptoms and signs of hypocalcaemia
muscle spasms in larynx, hands and legs
seizures
dental hypoplasia
long QT interval on ECG
someone who is chronically hypocalcaemia has an ECG. what will it look like
long QT interval
arrythmic
what are 2 examination tests to test hypocalcaemia
chvostek’s sign = tap facial nerve = spasm of facial muscle
Trouseau’s sign = inflate BP to 20mmHg above normal for 5 minutes, hand goes into spasm
explain chvostek’s sign
a test for hypocalcaemia
tap on the facial nerve near the ear
facial spasm of muscles
explain Trouseau’s sign
test for hypocalcaemia
inflate BP by 20mmHg above normal systolic pressure for 5 minutes
hand goes into spasm
what are some things to look out for for hypocalcaemia
history of neck surgery/scar
other autoimmune conditions
family history of hypocalcaemia
anti-epileptics
growth failure/hearing loss
what are the two main causes of hypocalcaemia
low magnesium (needed for PTH stimulation)
low vitamin D (activated in kidney to increase calcium absorption)
how do we treat hypocalcaemia (4)
if low vitamin D - give unactivated vitamin D
if low Mg = give Mg
calcium supplements
if surgery on thyroid/parathyroid then give activated vitamin D as PT is needed for activation
at what point does a hypocalcaemic patient become ‘severe’ and need IV calcium
<1.9mmol/mol
what are the main 2 causes of hypercalcaemia
primary hyperparathyroidism
myeloma/ bone mets/tumour in parathyroid gland
(drugs e.g. calcium drugs)
what are some causes of hypercalcaemia
primary hyperparathyroidism
myeloma/ bone mets/tumour in parathyroid gland
(drugs e.g. calcium drugs)
phaechromocytoma
immobilisation
lots of milk/alkali
thiazides
adrenal insufficiency
what are symptoms of hypercalcaemia
thirst
polyuria
nausea
constipation
confusion
what are symptoms of hypercalcaemia
thirst
polyuria
nausea
constipation
confusion
what are some consequences of hypercalcaemia
gastric ulcer
weak bone density/fractures
ECG abnormalatis short QT interval
renal stones
pancreatitis
what 4 medications must we look for in hypercalcaemia
thiazides (high BP)
lithium for mental health
calcium supplements
vitamin D
what is tertiary hyperparathyroidism and what causes it
where we get enlarged PT gland = hypercalcaemia
chronic kidney failure = low vit D (or just vit D deficency) = hypocalcaemia
leads to hyperplastic PT gland = tumour
= excess PTH and hypercalcaemia
why might kidne failure cause hypo and hypercalcaemia
chronic kidney failure = low vit D = hypocalcaemia
low calcium = hyperplastic PT gland = tumour
= excess PTH and hypercalcaemia
how do we check for parathyroid tumour in hypercalcaemia
check PTH levels
in normal, if calcium is high = low PTH
in tumour, if calcium is high = PTH also high
what causes primary hyperthyroidism
benign tumour / hyperplasia
if the pt has hyperthyroidism AND high PTH, what test do we do
24 hour urine calcium test
to determine if primary hyperparathyroidism OR FHH
what are the two differential diagnosis for hypercalcaemia and high PTH and how do we differentiate
primary hyperparathyroidism OR FHH
24 hour calcium urine test < 0.01mmol/L = FHH
24 hour calcium urine test > 0.01mmol/L = primary hyperparathyroidism
pt has hypercalcaemia. what tests do we do
PTH test
if high or normal = 24 hour urine test >0.01mmol/L is primary hyperparathyroidism and <0.01mmol/L is FHH
if low = malignancy,
what is FHH
familial hypocalcuric hypocalcemia.
This is a kidney problem.
The body retains calcium at the kidneys, raising the blood levels. This causes the PTH to drop.
what are the 4 consequences of primary hyperparathyroidism (oans)
BONEs (bone pain, osteoperosis, cysts in skull)
kidney STONES
physic GROANS - confusion
abdominal MOANS - constipation, acute pancreatisis
pt has a cyst in the skull, feeling confused and constipation. What might be the cause
primary hyperparathyroidism = hyperclacaemia
if a patient has hyperparathyroidism and is under 50, what do we do
surgery
how do we treat hyperparathyroidism if mild
FIRST CHECK PTH levels
surgery if indicated (e.g. <50 years old or severe symptoms)
if not indicated, monitor 2 times a year
how do we manage a hospitalised pt with hypercalcaemia
test blood for PTH!
normal IV saline solution for 5 hours
medications e.g. bisphosphonates (do XLA before this), cinacalcet, corticosteroids
Denosumab to prevent bone resoprtion
loop diuretics ONLY IF risk of overload
what medications can be used for hypercalcaemia (5)
bisphosphonates (do XLA before this)
cinacalcet (calcium receptor agonist)
corticosteroids (vitamin D toxins)
Denosumab to prevent bone resoprtion RANK-L Ligand
loop diuretics ONLY IF risk of overload
a patient is on cinacalcet , what are they being treated for
hypercalcaemia
when do we give loop diuretics to a hypercalcaemic patient
if at risk of fluid overload from saline
