Endocrinology Flashcards
(283 cards)
1
Q
what are the symptoms of hypercalcaemia?
A
confusion hallucinations stupor fatigue and easy tiring constipation muscle weakness (from slow muscle contractions) slow or absent reflexes
2
Q
what feature in a patient’s history may give signs of chronic hypercalcaemia?
A
a history of kidney stones
3
Q
what is the most classic sign of hypercalcaemia?
A
Slow or absent reflexes
4
Q
how does hypercalcaemia slow muscle contractions and reflexes
A
sodium channels are stabilised by calcium channels if there is excess calcium in the action potential is harder to reach meaning that neurons are less excitable
5
Q
what metabolic state does hypercalcaemia predispose to?
A
metabolic acidosis
6
Q
what features would you find on ECG of hypercalcaemia?
A
bradycardia AV block shortened QT interval
7
Q
how do you diagnose hypercalcaemia?
A
serum calcium levels > 10.5
8
Q
what are common causes of hypercalcaemia?
A
THe CHIMPANZEES
Thyrotoxicosis
Excess Vitamin D + A
C onsumption of calcium H ydration (dehydration) // hyperparathyroid I mmobilisation M yeloma (+leukaemias) P arathyroid cancer/ademoma A drenal insufficiency N eoplasm (Breast and lung + mets prostate) (thia) Z ide diuretics E thanol Excess PTH S arcoidosis
9
Q
what is the management of hypercalcaemia?
A
increase urinary excretion by using loop diuretics (frusemide) and increasing fluids + bisphosphonates to prevent bone resorption by inhibiting osteoclastsadj. glucocorticoids (beclamethosone) -> prevent bone resorption
10
Q
what little rhyme can help you remember the symptoms of hypercalcaemia?
A
stones bones abdominal moans , thrones and psychic groans
11
Q
what are common causes of hypocalcaemia?
A
HPV x2
hypoparathyroidism vitamin D deficiency hypo magnesium hyperventilation Phosphate infusions pancreatitis
12
Q
what are the uncommon causes of hypocalcaemia?
A
renal failure burns and sepsis
13
Q
w patient adjusted calcium comes back at <3mmol, are they likely to be symptomatic?
A
no
14
Q
what is the management of the patient who presents with serum calcium of 3-3.5
A
prompt treatment with fluids and bisphosphonates
15
Q
what is the management of a patient who presents the serum calcium of >3.5
A
urgent correction
fluids + diuretics (loop)
consider glucocorticoids
Bisphosphonates
16
Q
what is pseudo-hypocalcaemia?
A
hypocalcaemia caused by hypo albuminemia as there is less bound calcium but ionised Calcium is the same
17
Q
what are the symptoms of hypocalcaemia?
A
muscle cramps abdominal pain. Oral tingling seizures in extreme cases tetany with involuntary muscle contractions tachycardia brisk reflexes and abnormal ones paraesthesia numbness and tingling as well as poor memory and slowed thinking
18
Q
what is the effect of hypocalcaemia on action potential?
A
causes neuronal Destability allowing for easier depolarisation
19
Q
what abnormal reflexes can be seen in hypocalcaemia?
A
Chavatekes and Trousseuds
20
Q
what ECG changes can hypocalcaemia cause
A
arrhythmias such as atrial fibrillation prolonged ST segment and prolonged QT interval
21
Q
describe primary hyperparathyroidism
A
and endocrine disorder in which there is autonomous overproduction of parathyroid hormone resulting in deranged calcium homeostasis
22
Q
what are the usual causes of primary hyperparathyroidism
A
parathyroid adenoma - can also be caused by radiation and lithium therapy
23
Q
does hyperparathyroidism always cause high calcium?
A
now can also be normal cosmic despite high PTH
24
Q
as well as the normal symptoms for hypercalcaemia what else can be present in hyperparathyroidism?
A
bone pain easy fractures and a history of osteoporosis/osteopenia
25
what bloods should you perform in primary hyperparathyroidism
serum calcium ( norm/+) serum intact PTH (+) serum vitamin D levels norm/low) phostphate (-)
26
after bloods lead you to suspect hyperparathyroidism what further investigations should you perform?
head CT for underlying adenoma and DEXAscan for bone density
27
what is the management of primary hyperparathyroidism?
parathyroidectomy with adjuncts of: bisphosphonates vitamin D supplements and Cinacalet (helps reduce serum calcium)
28
what all the common causes of secondary hyperparathyroidism?
chronic kidney disease malabsorption syndromes low vitamin D and drugs
29
how does chronic kidney disease caused secondary hyperparathyroidism?
diminishes parathyroid hormone effect on kidneys mean there is less calcium absorption
30
how do malabsorption syndromes lead to secondary hyperparathyroidism?
less calcium absorption in the GI tract means that there will be access parathyroid hormone produced
31
what things can increase the metabolic requirement of calcium?
bisphosphonate and growing
32
what drugs increase calcium loss?
loop diuretics
33
how do you diagnose secondary hyperparathyroidism?
low serum calcium (+) serum intact parathyroid hormone (+) phasphate (+) vitamin D + finding any underlying cause such as doing coeliac testing, U+E, imaging of parathyroid gland
34
what can help manage secondary hyperparathyroidism?
dietary phosphate restriction and a phosphate binder
35
what are examples of phosphate binders?
calcium acetate or Sevelamer
36
what are the causes of low vitamin D?
using SPF avoiding the sun inadequate dietary intake obesity drugs and malabsorption
37
what drugs cause low vitamin D?
glucocorticoids antiepileptics HAART rifampicin
38
what does low vitamin D cause in children?
Ricketts
39
what x-ray findings would you see for Ricketts
widening of endo- epithelial plates of long bones and ragged poor mineralisation
40
what does low vitamin D causing adults?
can cause osteopenia osteomalacia and osteoporosis however usually it is asymptomatic with some lethargy and possibly proximal muscle weakness
41
what bloods would you need to perform for vitamin D deficiency?
vitamin D (-) alkaline phosphate (+ in rickets or psteomalacia ) serum calcium (- long standing low vD)
42
how do you manage vitamin D deficiency?
ergocalciferol sensible UV exposure calcium – calcium carbonate
43
the patient presents with some lethargy and proximal muscle weakness, you perform a blood test and noticed that vitamin D is low alkaline phosphate is raised and serum calcium is low what does this mean
there is vitamin D deficiency which has been a long-standing causing osteomalacia
44
what does a raised alkaline phosphate mean in context of low vitamin D?
Ricketts or osteomalacia
45
what does a low serum calcium mean in context of low vitamin D
long standing low vitamin D
46
what are the causes of hypoparathyroidism?
post surgical genetic autoimmune
47
what is meant by postsurgical hypoparathyroidism?
is one of: accidental removal of parathyroid glands vascular compromise transient and hungry bone syndrome
48
why does transient postsurgical hypoparathyroidism occur?
in hypercalcaemia due to hyperparathyroidism tissues have suppressed and once hyperparathyroidism is corrected and the core is removed it takes a while for the parathyroid tissues to return to normal function
49
what is hungry bone syndrome?
hypocalcaemia and hypophosphataemia occurring after thyroidectomy or parathyroidectomy
50
a patient presents with muscle cramps abdominal pain and tingling of the skin they have brisk reflexes so you perform a full blood screen on them you find serum calcium (-) albumin (norm) parathyroid hormone (-) magnesium (slightly +) vitamin D (-) phosphurus (+) - what is the most likely diagnosis?
hypoparathyroidism
51
described their blood test results that you would find on hyperparathyroidism
calcium (-) albumin (norm) PTH (- or norm) Magnesium (inhibits PTH secretion) vitamin D (-) creatine and phosphurus (+)
52
what is the management of hypoparathyroidism?
PO/ IV calcium + vitamin D- if not a enough add recombinant PTH - if you notice that calcium is being lost in the urine add thiazide diuretic
53
what other causes of hypomagnesaemia?
loop and thiazide diuretics long-term PPI use dietary and malabsorption syndromes acutely occurs after an MRI occurs in acute pancreatitis
54
how does hypomagnesaemia affect potassium and calcium?
potassium: potassium efflux is increased as it is normally inhibited by magnesium calcium: low magnesium causes high calcium as calcium release is normally inhibited by magnesium however low magnesium can also cause hypo para which would cause low calcium
55
how do you treat hypomagnesaemia
loading dose plus IV infusion of magnesium - make sure to check renal function and stop magnesium inclusion if you notice bradycardia or hypotension
56
what diseases are associated with posterior pituitary?
lack of vasopressin (cranial diabetes insipidus) resistance to action of vasopressin (nephrogenic diabetes insipidus) too much vasopressin (SIA DH)
57
if you notice hyponatraemia what is one of the first steps you should do
note serum osmolality and thenthe hydration status as it can indicate the cause of hyponatraemia
58
what are the three types of hypotonic hyponatraemia
hypovolaemic hypovolaemic ebovulaemic
59
what are the causes of hypovolaemic hyponatraemia?
GI fluid loss mineralocorticoid deficiency and dehydration
60
what are the causes of hypovolaemic hyponatraemia?
AKI/CKD CHF cirrhosis nephrotic syndrome
61
what are the causes of evovulaemic hyponatremia?
SEI ADH high fluid low so you or electrolytes which can occur in marathon running for example medications and adrenal insufficiency beer diets
62
what medications can cause Evovolumia hyponatremia?
thiazide like diuretics combination diuretics loop diuretics and ACE inhibitors anticonvulsants hormonal analogues such as desmopressin and oxytocin hypnotics such as temazepam recreational drugs such as ecstasy SSRI MAOI
63
describes the homeostasis of plasma osmolality?
osmolality gets too low thirst is suppressed and vasopressin is suppressed this dilutes your in increasing osmolality there is then negative feedback on the posterior pituitary
64
describe the renin angiotensin aldosterone system
when blood pressure is too low, or salt (NaCl) or circulating vol decreases the perfusion to the juxtoglomerlular apparatus decreases / this causes an increase on the production of renin by the kidneys/ renin converts angiotensinagen to angiotensin I/ ace is secreted by the surface of the pulmonary and renal endothelium which then converts angiotensin I --> angiotensin II / angiotensin II increases sympathetic activity increases tubular salt reabsorption and potassium excretion as well as water retention it causes the adrenal gland cortex to secrete furthera ldosterone which further propagate this / it causes arteriolar vasoconstriction causing an increase in blood pressure and an increase in the pituitary glands of posterior lobe antidiuretic hormone secretion causing water absorption from the collecting duct of the kidney all of this causes water and salt retention effective circulation volume increase and increases the perfusion of the juxta glomeruli apparatus which then causes negative feedback on the kidneys
65
what is the presentation of hyponatraemia?
mild cognitive symptoms: confusion headache and balance low in urine output, hypovolaemia and hyponatraemia dizziness fatigue nausea and profuse sweating hyponatraemia predisposes to seizures
66
what is a consequence of hyponatraemia occurring rapidly less than 48 hours
causes cerebral oedema
67
what is the presentation of cerebral oedema caused by hyponatraemia?
altered mental status seizures coma
68
what is the immediate management of cerebral oedema caused by hyponatraemia?
medical emergency requiring hypertonic 3% saline
69
after assessing volume status what is the next step in finding the cause of hyponatremia
checking urine sodium and urine osmolality
70
if a patient is hypervolaemic in the urine sodium is less than 20 what is the likely cause
heart failure cirrhosis or nephrotic syndrome
71
if the patient is hypervolaemic and the urine sodium is over 20 is the most likely cause?
chronic renal failure
72
the patient is Euvovolumic and the osmolality is high what is the most likely cause?
SIADH + drugs
73
the patient is Euvovolumic and the osmolality is variable what is the most likely cause?
prolonged exercise or high fluid intake
74
the patient is Euvovolumic and the osmolality is high what is the most likely cause?
primary polydipsia or potomania
75
the patient is hypovolumic and urine sodium is less than 20 what is most likely cause
non-renal sodium losses
76
the patient is hypovolumic and urine sodium is less than 20 what is most likely cause
renal sodium losses
77
for a patient to be evolaemic what should the urine sodium be like
over 20
78
if there is hyponatraemia and serum osmolality is high what the most likely causes
hyperglycaemia and hypertonic fluid administration
79
if there is hyponatraemia and serum osmolality is normal what is the most likely cause
pseudo-hyponatraemia is the most common cause of isotonic hyponatraemia
80
describes the steps of the investigation of hyponatraemia?
1. serum sodium
2. serum osmolality IF HYPOtonic
3. volume status
4. Urine sodium to assess cause
81
Apart from assessing serum osmolality and urine sodium what other tests should be performed in a person with hyponatraemia? And why?
glucose test – hypoglycaemia associated with low sodium thyroid function test – hypothyroidism needs to be excluded in order to diagnose NSAID H serum cortisol – excludes adrenal insufficiency serum lipids – high lipids means pseudo-hyponatraemia
82
What is the first step of management of acute hyponatraemia?
IV hypertonic saline line over 20 minutes regularly check sodium and repeat IV infusions of 3% hypotonia say line over 20 minutes until there is a 5mm/L increase in sodium
83
after you have managed to get sodium to increase by 5mmol/l what is the next step in the management of hyponatraemia?
stop infusion and start an IV line of not .9% say line on minimum volume find and manage the underlying cause
84
at what rate should sodium levels increase during the first 24-hour is after initial stabilisation? And what about after the first 24 hours?
increased to 10mmol/l and then an increase of 8mmol/lUNTIL 130mmol/l
85
how often should you check sodium whilst the stabilising hyponatraemia?
initially check after every IV infusion once initial stabilisation has occurred checked every six , 12 hours and then daily
86
what are the risks associated of to too rapid an increase in sodium in the management of hyponatraemia?
predisposes to central pontine myelinosis and cerebral oedema (causing osmotic demylination)
87
what is central pontine myelinosis
brain damage caused by pseudo-bulbar and pons demyelination in the cortico spinal and cortico bulbar tracts
88
what is the presentation of central pontine myelinosis
spastic quadriplegic confusion horizontal gaze paralysis mutism this is called locked in syndrome occurring over 48 – 72 hours
89
apart from medical management causing central pontine myelinosis what else can cause this?
beer potomania the rapid and consecutive drinking of bacon drop sodium very low leading to locked-in syndrome
90
what is SIADH?
syndrome of inappropriate antidiuretic hormone - too much antidiuretic hormone is secreted this impairs urinary excretion leading to fluid retention
91
where does antidiuretic hormone target in the kidneys?
the distal convoluted tubule and the collecting ducts is where there is the actual antidiuretic hormone causing fluid retention
92
what type of hyponatraemia does SIADH cause?
evolumic hypotonic hyponatraemia
93
what is another name for antidiuretic hormone
vasopressin
94
what are causes of SIADH?
malignancy including SCLC GI pulmonary infections CNS disorders such as infections MS GBS drugs such as SSRI amitriptyline amiodarone carbamazepine
95
if you suspect SIA DH what blood test must you perform in order to get the diagnosis?
after finding out the type of hyponatraemia by using serum osmolality and urine sodium check diode function and serum cortisol as SIA DH is a diagnosis of exclusion
96
how do you manage S IAD H
treat hyponatraemia with acute treatment and chronic management
97
what is a chronic management of hyponatraemia
loop diuretics if caused by chronic heart failure own erotic syndrome Spironolactone caused by cirrhosis vasopressin receptor agonists are usually used second line
98
what is the definition of hyprenatraemia
serum sodium concentration of over 145 mmol /l
99
what other three types of causes of hypernatraemia
free water loss deficit in water losses sodium losses
100
what is the most common cause of hypernatraemia
dehydration
101
what is meant by free water loss causes of hypernatreamia
GI losses insensible losses and sweat renal concentrating defects osmotic diuresis diabetes insipidus
102
what is meant by deficit in water losses causes of hypernatraemia?
inability to drink water impaired thirst mechanism from brain tumours general lack of drinking
103
what is meant by sodium losses causes of hypernatraemia
hypertonic fluids excess sodium ingestion mineralocorticoid excess in Cushing's or primary aldosteronism
104
in severe hypernatremia what is a consequence of its
acute cerebral shrinking
105
what is the presentation of hypernatremia
feelings of thirst weakness nausea and loss of appetite if more severe muscle twitching confusion + intracranial haemorrhage
106
which individuals most at risk of developing hypernatremia
patient of older age especially if living in a care home as they tend to get hypovolaemic
107
what investigation should you perform in hypernatremia?
U+E -? Renal impairment urine osmolality serum osmolality urine electrolytes and outputs
108
if urineosmolality is High Street higher than plasma osmolality what is the most likely aetiology
pure volume depletion from GI or insensible losses
109
if urine osmolality is the same as plasma osmolality what is the most likely cause
renal concentration defects such as renal failure osmotic diuresis or use of diuretics
110
what is the management of hypernatremia
give IV fluids loop diuretics if caused by yet eugenic causes or mineralocorticoid excess this is usually the case if the patient is hyper volumic
111
what is diabetes insipidus
metabolic disorder characterised by the inability to concentrate urine
112
what is the classic triad associated with diabetes insipidus
inapropiately dilute urine polyuria polydipsia
113
what are the two types of diabetes insipidus
central and nephrogenic
114
describe central diabetes insipidus
has an absolute or relative deficiency of AVP causing a reduced permeability of ducks within the nephron towards the reducing water resorption and increasing water loss
115
what are some causes of central diabetes insipidus
pituitary surgery can be transient or long lasting crania for NGO ma post traumatic head injury due to lesions CNS infections vascular compromise – subarachnoid haemorrhage phenytoin or congenital/genetic mutations
116
describe nephrogenic diabetes insipidus
renal and sensitivity or resistance to AVP reducing the permeability of ducts within the nephron to water reducing water resorption and increasing water loss
117
what are some causes of nephrogenic diabetes insipidus
lithium gentamicin rifampicin systemic disease electrolyte abnormalities kidney disease obstruction
118
what is an important measurement in the investigations of diabetes insipidus
measuring urine volume diabetes in separatists is unlikely if your volume is less than 3 L
119
what is the electrolyte abnormality of diabetes insipidus
hypernatremia - any other electrolyte abnormalities suggests a different diagnosis
120
describe the findings of urine and serum osmolality in a patient with diabetes insipidus
serum osmolality is raised and urine is low
121
deviations and diabetes insipidus always have to be hypernatraemia
now sodium levels can be normal if they are managing to appropriately rehydrate
122
what is a diagnostic test for diabetes insipidus
water deprivation test
123
describe the results of the water deprivation test in diabetes insipidus
by starving a patient of water the normal physiological response is to keep the plasma osmolality equal but increase your in osmolality in diabetes insipidus the urine osmolality will remain on concentrated i.e. low
124
how do you differentiate between central and nephrogenic diabetes insipidus
desmopressin challenge test
125
describe a desmopressin challenge test and its results
by giving desmopressin you can differentiate between central and nephrotic because in central the euro and osmolality will increase as a VP will increase however in nephrogenic urine osmolality will stay the same as the kidneys remain insensitive to AVP
126
after correcting hyponatraemia with fluids what is the management of diabetes insipidus?
Central: give desmopressin peripheral: sodium restriction and thiazide diuretics treat any underlying causes
127
what are the types of adrenal insufficiency?
primary - adrenal cortex failure secondary pituitary or hypothalamus tertiary chronic glucocorticoid administration
128
what other symptoms of adrenal insufficiency
fatigue lack of energy weight loss tan on skin postural hypotension cramps in legs
129
what feature of adrenal insufficiency would you find primarily in primary adrenal insufficiency
skin pigmentation especially on palms scores and mucosa
130
when would you find alabaster pale skin pigmentation in the context of adrenal insufficiency
if secondary: pituitary or hypothalamus
131
how does adrenal insufficiency cause postural hypotension
mineralocorticoid or glucocorticoid deficiency causes this
132
why is primary adrenal cortex failure dangerous
involves all the steering production reducing it so blood pressure and U+E are not properly regulated
133
what features of an adrenal crisis
abdominal pain abdominal tenderness guarding and vomiting fever confusion somnolence delirium coma
134
what electrolyte abnormalities might be present in adrenal insufficiency
hyponatraemia hyperkalaemia possibly hypercalcaemia
135
Howard ran in and out this year own levels change in adrenal insufficiency caused by cortex failure
increase in running decreasing out the steering
136
what is a diagnostic test for adrenal insufficiency
morning cortisol - if less than 350 adrenal insufficiency is probable greater than 430 is unlikely to be an adrenal crisis
137
after you note that morning cortisol is low what further diagnostic test should be performed in the context of adrenal insufficiency
ACTH stimulation test a.k.a. short synactin test
138
describes ACTH stimulation test
ACTH is injected and the amount of cortisol produced is measured in primary there is no response (the adrenal cortex itself cannot make the cortisol) in secondary if it is not too severe there will be an increase in cortisol as pathology is in the tutorial hypothalamus
139
what is the management of adrenal insufficiency
ongoing glucocorticoid and mineralocorticoid replacement
androgen replacement therapy if decreased libido
140
what is an adrenal crisis
extremely low value of cortisol bare mind in the context of physiological stress a value of less than 500 nmol/l is diagnostic
141
what is the treatment of adrenal crisis
IN hydrocortisone 100 mg followed by 200 mg infusion over 24 hours plus IV .9% saline
142
what patient education regarding adrenal crises should be given to patients with adrenal insufficiency
the six-day rule if unwell double the dose of PO glucocorticoids parenteral administration during prolonged vomiting or diarrhoea and give an emergency hydrocortisone kit
143
described Cushing's syndrome
the clinical manifestation of pathological hypercorticonsim from any cause.
144
what all causes of Cushing's
pituitary adenoma, adrenal adenoma exogenus causes alcoholism physiological stress pregnancy and malnutrition
145
what is the physical presentation of Cushing's?
a.k.a. facial plethora acne thinning hair main face increased facial hair easy bruising weight gain purple striae pendulous abdomen slow wound healing swelling of feet/legs a.k.a. peripheral oedema in arms and legs with weak bones supra-clavicular fullness a.k.a. buffalo hump
146
what are the signs of Cushing's
hypertension poor short-term memory. Even see poor concentration menstrual irregularity glucose intolerance headaches insomnia prepare an infection and depression
147
how does Cushing's tend to present in children
may have pubertal abnormalities
148
how do you diagnose Cushing's?
serum and urine cortisol will be elevated first-line diagnostic test is late night library cortisol
149
if cortisol is increased what is the next investigation which you should perform and you suspect cushings?
dexamethasone suppression test
150
describe the dexamethasone suppression test
1 mg of dexamethasone overnight and early morning cortisol is measured. In people without Cushing's cortisol should be below as dexamethasone suppresses ACTH however in individuals with cuttings cortisol will remain high
151
A patient presents with
increased fat on your chest and tummy, but slim arms and legs
a build-up of fat on the back of your neck and shoulders, known as a "buffalo hump"
a red, puffy, rounded face
you run serum cortisol and it comes back +++
whats your next Ix?
pituitary MRI or adrenal CT to check for pituitary or adrenal adenoma
152
describe the HPA axis
hypothalamus secretes corticotropin releasing hormone which stimulates the anterior pituitary to release adrenocorticotropic hormone which stimulates the adrenal cortex to produce cortisol which has negative feedback on the hypothalamus's production of CRH and the pituitary production of ACTH
153
what is the management of Cushing's syndrome?
if endogenous surgery for the tumour medical therapy can be used to surgery is not yet advised or contraindicated and is used in the interim period between diagnosis and surgery - somatostatin analogues are used (pasireotide)
154
what is supposed surgical management of a patient who underwent surgery for Cushing's disease?
steroids given for about a week after surgery then if total pituitary removal has occurred give levothyroxine testosterone if male oestradiol and medroxyprogesterone for female consider giving somatotropin and desmopressin necessary
155
what is a prolactinoma
one of the most common types of pituitary adenoma, accounting for 40% of all pituitary adenomas is more common in females
156
what features of prolactinoma typical for females
amenorrhoea and galactorrhea
157
what features of a prolactinoma typical for males
erectile dysfunction hypogonadism and gynaecomastia
158
what are the classic symptoms of a pituitary adenoma/prolactinoma
visual disturbances by temporal hernia nuclear osteoporosis headaches and loss of libido + sex organ fueatures
159
here is more likely to present between postmenopausal and premenopausal women with a prolactinoma and why
premenopausal women are more likely to present earlier because they will experience early symptoms of a prolactinoma which on menstrual irregularities everyone else will present later when this starts to become compression of the optic hires and causing visual disturbances
160
what investigations are diagnostic for a prolactinoma
serum prolactin (+++) pituitary MRI
161
what is a management or prolactinoma
dopamine agonist ---> surgery and radiotherapy ( presurgery you can add a COC key to control symptoms of a prolactinoma in premenopausal females)
162
What is PCOS
defects in the HP PA access causes hyper- androgynous them through ovaries and adrenal glands causing a variety of symptoms including infertility
163
what are the symptoms of PCOS
hertuism acne infertility regular menses weight gain hypertension
164
what blood tests should be performed in ?pcos
serum prolactin(norm or +) serum testosterone (++) FSH (norm or - )and LH (+) fasting glucose (norm or +) fasting lipids(+)
165
what blood test should be performed in PCOS to exclude differentials? And what are those differentials?
Serum 17 hydroxy progesterone – excludes adrenal hyperplasia where it would be elevated serum TSH – excludes thyroid dysfunction
166
what is the management approach to PCOS?
manage the symptoms of PCOS such as infertility irregular periods acne hirtuism
167
after finding blood results which are indicative of PCOS what further investigation would you perform
pelvic ultrasound scan: polycystic ovaries in 75% of patients
168
what is the diagnostic criteria for PCOS
two out of three features of: irregular periods features of hyper androgenism (+/- lanb confirmation) ovarian cysts on ultrasound
169
how would you manage infertility in an individual with PCOS
encourage weight loss if there is a high BMI --> clomiphene (+adj Metformin +/- dexamethasone +/- spironolactone) --> gonadotropins --> IVF
170
how would you manage dysmenorrhoea in PCOS
cyclic progestin (then USS to measure endometrial thickness if normal roceed otherwise biospy for?endomerial cancer) --> COCP/ IUS/ POP ---> metformin
171
how you manage acne in PCOS
COCP --> top Abx --> top retinoids etc (Mx for acne vulgaris)
172
how do you manage hyperandrogenism in PCOS
COCO ---> antiandrogen ---> combination therapy --> GnRH + COCP (adj. metfirmin all way through can be added)
173
how does clomiphene work
helps release more FSH and LH thus inducing ovulation
174
how does Spironolactone work in terms of PCOS management
has antiandrogen properties
175
how does metformin work in terms of PCOS
reduces insulin levels and helps weight loss reducing testosterone levels and also helps stimulate monthly periods
176
what drugs can cause weight gain
diabetic therapies: insulin metformin psychiatric: TCA SSRI lithium atypical and typical antipsychotics mood stabilisers plus carbamazepine and gabapentin / corticosteroids/ hormonal contraception / NSAIDs antihistamines especially diphenhydramine beta-blockers ACE inhibitors ARB calcium channel blockers
177
what drugs can cause hertuism
anabolic steroids metoclopramide Meath although part progestins phenothiazines testosterone
178
what is the difference between hirtuism and hypertrichosis
the excessive growth of hairs on androgen -dependent areas is heirtuism generalised overgrowth of her everywhere is hypertrichosis
179
what drugs can cause hypertrichosis
cyclosporine hydrocortisone minoxidil penicillamine phenytoin streptomycin
180
what value of hyperkalaemia is considered severe
>6
181
what other symptoms of hyperkalaemia
muscle weakness fatigue and arrhythmias which can be fatal
182
what other ECG changes which you would see on hyperkalaemia
loss of P wave tall peaked T waves widen to QRS
183
what are the causes of hyperkalaemia
excessive potassium intake ineffective potassium renal excretion from renal impairment hormonal causes intracellular potassium release medications pseudo-hyperkalaemia
184
what are the causes of pseudo- hyperkalaemia
haemolysis during venipuncture thrombocytosis leucocytosis polycythaemia
185
what other medications which cause hyperkalaemia?
ACE inhibitors Spironolactone NSAID cyclosporinetracolimus trimethoprim heparin
186
what are the hormonal causes of hyperkalaemia
Addison's congenital adrenal hyperplasia of the steering deficiency
187
how do you treat hyperkalaemia
insulin and Ivy glucose unless there are severe arrhythmias then add calcium gluconate (doesn't change potassium but stabilise the heart)
188
how do ACE inhibitors cause hyperkalaemia
lowers aldosterone leading to decreased potassium excretion
189
how does congenital adrenal hyperplasia or aldosterone deficiency cause hyperkalaemia
leads to loss of aldosterone causing decreased potassium excretion
190
how does the spironolactone cause hyperkalaemia
it is a potassium sparing diuretic
191
how does Hartmann's solution because hyperkalaemia
contains potassium
192
what all causes of hypokalaemia
increased other steering diuretics hypomagnesaemia renal tubular acidosis metabolic alkalosis decrease oral intake vomiting or diarrhoea fistulas insulin alkalosis
193
how does insulin cause of hypokalaemia
drives potassium into cells
194
what is hypothyroidism
a clinical state resulting in the under production of thyroid hormones T4 and T3
195
describe secondary hypothyroidism
failure of the anterior pituitary to release TSH
196
what are causes of hypothyroidism
autoimmune – Hashimoto's (most common) thyroidectomy radiotherapy radioactive iodine therapy (using graves or nodular goitre) infiltrative disease such as sarcoidosis drugs
197
what drugs cause hypothyroidism
lithium amiodarone + others not v common
198
describes the thyroid hormone axis
the hypothalamus produces TR H which stimulates the pituitary gland to release TSH which causes the thyroid gland to produce T4 and T3 any teeth for produced is converted in the peripheral tissues to T3 high levels of T4 and T3 was negative feedback on both hypothalamus and pituitary
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describes the process of making thyroxine from thyroid follicles
a sodium iodine co-transporter transports sodium and iodine from the blood into the thyroid follicle the endoplasmic reticulum causes thyroglobulin secretion which then through XO psychosis is transported out of the thyroid follicular cell iodine moves through the thyroid follicular cell and through a pendrin transporter is transported out of the thyroid follicular cell into the follicle colloid where it is oxidised and joins with the thyroglobulin which has been released after this conjugation it moves from the follicle colloid back into the thyroid follicular cell to endocytosis through proto-losses it is cleaved into two molecules one of which is thyroxine this is then transported out through a transporter into the blood
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what are some transient causes of hypothyroidism
subacute granulomatous thyroiditis postpartum lymphatic thyroiditis
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what are the symptoms of hypothyroidism
weakness lethargy cold sensitivity constipation weight gain depression menstrual irregularity myalgia trial course gain eyelid oedema facial thickening thick tongue because her deep voice bradycardia delayed relaxation of tendon reflexes and rarely a goitre
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how do you investigate hypothyroidism
measure serum TSH and T4 also measure antithyroid peroxide antibodies (autoimmune cause such as Hashimoto's)
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why is doing a U+E important in hypothyroidism
can cause hyponatraemia
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what is the management of hypothyroidism
levothyroxine unless it is a subclinical value or there is a history of coronary artery disease then gave low dose levothyroxine
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what is a myoxedemic coma?
a rare but life-threatening disorder caused by decompensated hypothyroidism
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what usually triggers a myoxedemic coma?
infection especially lung and urinary stroke surgery trauma drugs
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what are the symptoms of myoxedemic coma?
weakness hypothermia facial Tonga and lower leg oedema hypotension reduced consciousness hypercapnia progressing to hypocapnia and myoxedema
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what test should you always perform in myoxedemic coma?
thyroid function blood glucose and U+E for hyponatraemia
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what is the management of myoxedemic coma?
IV fluids and eelectrolyte correction IV thyroid hormone and cortisol mad blood glucose and hypothermia - hyponatraemia merged with hypertonic saline
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what is the most common cause of hyperthyroidism
graves disease
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what is Graves' disease
and autoimmune condition attacking thyroid gland where TSH receptor antibodies because of overproduction of iodine and thus thyroid hormone
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what are causes of hyperthyroidism
graves toxic multi-nodular goitre iodine amiodarone
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how do toxic multi-nodular goitres cause hyperthyroidism
rogue nodules produces excess T3 and T4 or there is an adenoma secreting T3 and T4 this is known as a toxic adenoma
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how does excess iodine intake cause hyperthyroidism
used in thyroid synthesis (can be found in radio contrast agents)
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how does amiodarone cause hyperthyroidism
destruction of the thyroid cells and thyroiditis causing leakage of thyroid hormone
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what is the presentation of hyperthyroidism
weight loss tachycardia anxiety tremor heat intolerance sweating diarrhoea protruding eyes menstrual disturbances palpitations hair loss
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on examination what features may you find in tacky cardiac
enlarged thyroid gland or goitre lid lag incomplete eye movements due to orbitopathy
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if on examination you find a diffuse goitre what does this indicate
Graves' disease
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what blood tests should you perform for hyperthyroidism
TSH (-) T3 T4 (+) TSH receptor antibodies (Graves)
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after finding increased levels of T3 T4 and decreased levels of TSH on a blood test what further investigations should you do
check for antibodies then also do a radioactive I dine or technetium scan or a thyroid ultrasound scan
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what would radioactive iodide or technetium scan show in hyperthyroidism
increased generalised uptake of radioactive iodine quartet nation shows grades if however uptake is in multiple focal spots it shows multi-nodular goitre focal spot shows adenoma thyroiditis or leakage would show uptake outside of the thyroid
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what is the management of hyperthyroidism
start symptomatic therapy of propranolol ( can use radioactive iodinebut this is used in pregnancy )ongoing management with carbimazole , surgery is used if there is relapse after trial of carbimazole
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what is the principle of management with carbimazole in
either titrate the dose up until you reach satisfactory T3 T4 or completely block the production of T3 T4 (this is done in Graves' disease and then replace with thyroid hormone) after a course of treatment stop and sometimes it goes back to normal
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what drug is required in a thyroid storm?
propylthiuracil
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how would you treat orbitopathy/ thyroid disease
methylprednisolone
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describe thyroid disease
condition in which the eye muscles eyelids to glance in fatty tissues behind eyes become inflamed
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describe pre-tibial myexodema
skin manifestation of graves due to infiltrative deposition caused by the autoimmune nature of the disease
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what is acropathy
a dermopathy associated with Graves' disease it is characterised by soft tissue swelling of the hands and clubbing of the fingers
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what are side effects of thionamides
are generally well tolerated but commonly cause a rash and less commonly cause arthralgia hepatitis neuritis thrombocytopenia and vasculitis symptoms usually occur within the first few months but resolved after stopping the drug
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what is thyrotoxicosis
extreme hyperthyroidism
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what is the management of thyrotoxicosis
high dose propylthiouracil I the hydrocortisone, esmolol Iv or immidiate relese propranolol + lugol solution
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what is lugol solution
iodine/potassium iodide used to avoid exacerbations
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how can cholestryramine help in thyrotoxicosis
helps reduce enterohepatic circulation of TSH and reduces thyroid hormone secretion
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what is acromegaly
a rare chronic disease caused by excessive secretion of growth hormone usually due to pituitary somatotropin adenoma
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what usually causes acromegaly
pituitary tumour
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what is the presentation of acromegaly
profuse sweating acral growth coarsening of facial features and a history of carpal tunnel syndrome, arthralgia, glucose intolerance or diabetes, amenorrhoea hypertension and sleep apnoea may be present
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what is the picture below show
acromegaly
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describes theHPG axis
hypothalamus produces GHRH this stimulates the pituitary to produce growth hormone HRH the hypothalamus is also stimulated by Ghrelin produced by the stomach in response to stress amino acids or hypoglycaemia. GH produced by the pituitary goes to the muscles adipose tissue producing free fatty acid growth plates and liver the growth plate and liver produce IGF one which causes cell differentiation and proliferation and also causes negative feedback on the pituitary and hypothalamus growth hormone also produces negative feedback on the hypothalamus and somatostatin also produces negative feedback on the hypothalamus
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described the blood tests required in acromegaly
measure IGF -! (++) be aware that other states like adolescents also increase this GH (++) OGTT can be raised if the growth hormone levels are normal on blood test an abnormal GTT can be partially diagnostic
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after performing blood tests for acromegaly what is the next step in the diagnosis
pituitary MRI or CT finding the underlying cause
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what is the management of acromegaly
surgical but somatostatin analogues can be used to reduce hypothalamic GHRH ( they are GHR agonists) dopamine agonists can be used as adjuncts to increase IGF responsiveness
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how does anabolic steroid use affect the HPT - gonad axis
testosterone is responsible for adrenergic and anabolic functions it causes negative feedback on the axis and suppresses GNR HLH and FSH, anabolic steroids
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what are male features of anabolic steroid use
testicular atrophy decreased sperm count and motility impotence acne and oily skin irreversible gynaecomastia high voice
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what are the female features of anabolic steroid use
acne and oily skin menstrual abnormalities changes in libido hirtuism male pattern baldness deep voice clitoral hypertrophy
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what are endocrine myopathies
hormonal imbalances causing atrophy and muscle weakness mainly causing proximal myopathy
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what are symptoms of endocrine myopathies
muscle stiffness cramps slowed reflexes and in severe cases muscle breakdown
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what are the most common causes of endocrine myopathies
hyper and hypothyroidism and parathyroid disorder
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how does hyperthyroidism cause proximal myopathies
thyroxine in excess is toxic to neuromuscular junctions
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how does hypothyroidism cause proximal myopathies
not well understood - to do with thyroxines role in metabolic cellular function leading to abnormal gluconeogenesis and insulin resistance leading to muscle atrophy
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how does parathyroid disorder cause proximal myopathies
causes hypercalceamia + hypomagnesemia which leads to proximal myopathy
251
what are carcinoid syndromes
XS seratonin and other vasopeptides are released from carcinoid tumoir
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where do most carcinoid tumours occur
midgut neuroendocrine tumours
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what does the picture below show
facial flusching associated with carcinoid tumours
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what is the common presentation of carcinoid tumours
facial flushing diahhorea which is v long standing (years) plus… tachycardia abdominal cramipng and signs of RSHF
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what does RSHF mean in the context of carconoid tumours
that cardinoid heard disease is occuring
256
how do you diagnose carcinoid syndrome
imaging and biopsy + urinary 5 hydroxyindoleacelic acid (++) - an indicative factor
257
What is Conns disease?
aka Primary aldosteronism. A common and specifically treatable cause of hypertension
258
What is the pathophysiology of primary aldosteronism?
XS aldosterone means there is XS sodium (+ Cl-, K+ excretion and H2O is retained in tubule so XS urine) reabsorbtion leading to hypertension and decreased RAAS activation
259
What metabolic abnormalities does Conns disease cause?
hypernatremia, hypokalemia (metabolic acodosis!!)
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What is the presentation of Conns disease?
Hypertension and strong family history of hypertension Nocturia and polyuria + symptoms of hypernatremia - irritability difficulty concentrating, anxiety depression, feelings of thirst, --> muscle twitching and confusion
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what is the diagnostic investigation of Conns disease?
aldosterone/renin ratio with confirmation using fludrocortisone suppression test
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describe the fludrocortisone suppression test?
fludroCortisone administered over four days then upright plasma aldosterone is measured if there is failure to suppress the steering and plasma cortisol is lower at 10 AM then it is at 7 AM with correction in potassium then it is a positive diagnosis for conns disease
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why does plasma cortisol have to be lower at 10am than 7 AM to be a positive diagnosis for conns disease?
because acute ACTH rise from another pathology prevents aldosterone suppression (so wouldn’t be 1ry hyperaldosteronism)
264
after a positive fludrocortisone test what is the next step in the investigation for Conns?
Adrenal CT - aldosterone producing tumour / genetic testing - familial PA
265
what is the management of conns?
spironolactone - aldosterone antagonist + surgery if applicable
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what drugs cause hirtuism?
anabolic steroids / testosterone/ glucocorticoids / cyclosporin/ phenytoin
267
What is pituitary apoplexy
infarction or haemorrhage into a pituitary tumour which causes extremely low levels of ACTH and cortisol
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what is the biggest risk of pituitary apoplexy
acth and cortisol can cause circulatory collapse
269
what is the presentational pituitary apoplexy
the presentation is similar to a subarachnoid haemorrhage
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what structures would surround the pituitary gland and could get compromised in pituitary apoplexy
optic nerves lateral to the pituitary and the chiasm is superior
271
what is the investigation is required for pituitary apoplexy
pituitary screen and CT head may be needed as Px is similar to SAH
272
what is tested in a pituitary screen
LH FSH TSH T4 T3 cortisol prolactin ACTH- if possible
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what is the first line management of pituitary apoplexy
IM/Ivy hydrocortisone for adrenal failure which occurs in apoplexy
274
what is a pheocytochroma?
tumour arising from the catecholamine producing chromaffin cells of the adrenal medulla
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what do chromaffin cells of the adrenal medulla produce
adrenaline and noradrenaline and rarely dopamine
276
who is a typical patient which gets a pheocytochroma?
young adults/teenagers
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What is a presentation of a pheocytochroma?
headaches palpitations diaphoresis hypertension very high which is sustained and paroxysmal
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what is a consequence of pheocytochroma?
hypertensive retinopathy
279
what is a first line management for suspected pheocytochroma?
ASAP alpha blockers - phentolamine until BP is stabalised
280
what is contraindicated in the acute management of pheocytochroma?
beta-blockers in the acute phase of the management of pheocytochroma beta-blockers or worsen the hypertension
281
what is the ongoing management of pheocytochroma?
alpha blocker and beta-blocker hydration and a high salt diet ( can give adjacent calcium channel blocker) definitive management is with surgery
282
how would you diagnose a pheocytochroma?
24-hour urine collections of catecholamines genetic testing required to rule out SD HB MRI/CT
283
in an acute presentation of pheocytochroma what test should you do?
serum free metanephins and normetanephins (both +++) +/- CT
