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endo conditions Flashcards

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1
Q

primary hyperparathyroidism presentation

A

-most cases are asymptomatic and diagnosed incidentally on blood test where hypercalcaemia is detected

  • symptom mneumonic is: bones, stones, abdominal groans and psychic moans + polydipsia, polyuria
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2
Q

primary hyperparathyroidism bloods findings

A

hypercalcaemia
low phosphate
normal or high PTH

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3
Q

top causes of primary hyperparathyroidism

A

solitary adenoma 85%
10% hyperplasia and other stuff less %

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4
Q

pathophysiology of secondary and tertiary hyperparathyroidism vs primary

A

primary (for the causes listed in other card) PTH goes up first and that leads to ca+ going up and Phosphate to drop
vs

secondary means that the PTH rises DUE TO A ALREADy existing LOW CALCIUM- ex CKD or other kidney problem ect

TERITIARY is basically when secondary has lasted for so long that the parathyroid is so used to overproducing PTH due to the chronically low Ca that it ends up starting to produce PTH even when Ca normalises.

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5
Q

lab finding differences between primary secondary and tertiary hyperparathyroidism

A

primary and tertiary: high PTH, high Ca difference is CKD usually in tertiary and low vit d potentially

secondary: high pth low calcium and low vit d

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6
Q

associated conditions with primary parathyroidism

A

MEN
and hypertension

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7
Q

xray findings in primary hyperparahtyroidism

A

pepperpot skull
osteitis fibrosa cystica

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8
Q

treatment of primary hyperparathyroidism

A

definitive treatment is with total parathyroidectomy

conservative management if 1) calcium only 0.25 mmol above normal range 2) >50 yo 3) no evidence of end organ damage

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9
Q

non surgical treatment option for patience not suitable for surgery with primary hyperparahtyroidism

A

cinacalcet, a calcimimetic
‘mimics’ the action of calcium on tissues by allosteric activation of the calcium-sensing receptor

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10
Q

diagnosis of type 2 diabetes

A

if with glucose:
symptomatic and fasting > 7 and random > 11 and if asymptomatic this needs to be in 2 separate occasions

if with HBA1C > 48 is diagnostic but needs to be done twice if asymptomatic!!!!

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11
Q

what is Impaired fasting glucose and what to do about it

A

when fasting glucose is 6.2-7 and you do a glucose challenge which needs to be <11 for no diabetes confirmation

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12
Q

first line management of diabetes

A

metformin ONLY
and you need SGLT-2 as well if CVD OR RISK OF CVD OR HF but start the sglt2 after theyre established on metformin

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13
Q

targets of hba1c with diabetes

A

48 if on lifestyle or lifestyle+ metformin and 53 if on a drug that may cause hypoglycaemia such as sulfonyluria

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14
Q

what to do if patient is not meeting the target and hba1c <58

A

you increase metformin from two to 3 times daily and stronger lifestyle factors

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15
Q

when do you need to add a second drug?

A

if hba1c> 58

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16
Q

what drugs can you add as second line?

A

DPP-4 inhibitor
pioglitazone
sulfonylurea

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17
Q

if patient doesnt achieve control in 2 drugs?

A

metformin + DPP-4 inhibitor + sulfonylurea
metformin + pioglitazone + sulfonylurea
metformin + (pioglitazone or sulfonylurea or DPP-4 inhibitor) + SGLT-2 if certain NICE criteria are met
insulin-based treatment

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18
Q

what if triple therapy not enough?

A

If triple therapy is not effective or tolerated consider switching one of the drugs for a GLP-1 mimetic:
BMI ≥ 35 kg/m² and specific psychological or other medical problems associated with obesity or
BMI < 35 kg/m² and for whom insulin therapy would have significant occupational implications or weight loss would benefit other significant obesity-related comorbidities
only continue if there is a reduction of at least 11 mmol/mol [1.0%] in HbA1c and a weight loss of at least 3% of initial body weight in 6 months

GLP-1 mimetics should only be added to insulin under specialist care

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19
Q

advice on starting insulin for t2d?

A

metformin should be continued. In terms of other drugs NICE advice: ‘Review the continued need for other blood glucose-lowering therapies’
NICE recommend starting with human NPH insulin (isophane, intermediate-acting) taken at bed-time or twice daily according to need

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20
Q

diabetic neuropathy PRESentations

A

loss of sensation and neuropathic painnn (pins and needles, shock-like pain) in a glove and stocking distribution, not loss of movement

GI autonomic neuropathy: gastroparesis, chronic diarrhoea, GORD

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21
Q

treatment of diabetic neuropathic pain first and second line

A

same as other neuropathic pain, one of: amitriptyline (TCA), gabapentin, pregabalin (ANTIEPILEPTICS), duloxetine (snri) ,

second line: adding another one from that list

pain management clinic for severe

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22
Q

LOcal neuropathic pain management eg after herpes infection

A

local capsaicin

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23
Q

acute neuralgia/ exacerbation treatment

A

tramadol

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24
Q

presentation/ pathophysio of gastroparesis

A

basically hypomotility of GI tract, leads to
1) erratic control of blood glucose (bc it moves weirdly so absorption can be delayed: big drop glu and then when it suddenly empties: spike in glu)

2) vomiting, bloating

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25
treatment of gastroparesis
prokinetic agents eg. metoclopramide, erythromycin, domperidone
26
GORD pathophysiology in diabetic autonomic neuropathy
reduced lower oesophageal sphincter pressure
27
diabetic nephropathy presentation
lke CKD a bit, proteinuria, hypertension, progressive decline in GFR and can lead to ESRF (end stage renal failure)
28
screening for diabetic nephropathy
annual screening, ACR measured- MORNING (first wee) measurement
29
pathophysiology of diabetic nephropathy
hyperglycaemia induced damage to renal microvasculature: glomeruloscleritis, tubulointerstitial fibrosis
30
management of diabetic nephropathy
very good glycemic control, antihypertensives keep bp under 130/80 ACEi or ARB if ACEi >3 low protein intake dyslipidaemic control: statins
31
type one diabetes differences to type 2 on presentation
generally commonly presents as DKA So rapid onset- hours/ days vs weeks / months in t2d recent weight loss typical DKA symptoms vs milder in T2D - polydips and polyur. ketonuria younger (<20 but 40% Are > 30!!! so not totally)
32
features of DKA
ABDO PAIN dehydration polydipsia polyuria kusmail respiration - deep hyperventilation acetone smelling breath
33
initial investigations when someone is presenting with first time t1d aka DKA
urine dip for glucose and ketones and fasting and random blood glucose
34
what investigation helps distinguish t1d from t2d
diabetes specific antibodies and C- peptide since its LOW in t1d and high in t2d
35
which investigation is NOT useful for a patient with suspected T1D
HbA1c as it may not reflect the rapid rise in glucose
36
most common T1D ab
anti-GAD glutamic acid decarboxylase
37
most common t1d ab in young children
insulin autoantibodies IAA (only 60% of patients have it later on)
38
other common antibodies in t1d
Islet cell antibodies ICA and insulinoma associated 2 antibodies
39
diagnostic criteria for t1d
fasting glucose> 7 and random glu > 11.1 and symptomatic if not symptomatic the two glucoses need to be demonstrated on 2 separate occasions
40
monitoring aspect of t1d management
hba1c every 3-6 months adult target < 48 but take into account the individual self monitor blood glu min 4 times before meals and bed and more if ill or during and before after sport, pregnancy breastfeeding ect 5-7 on waking 4-7 all other times
41
medical management of t1d
best regime is multiple daily injection basal / bolus regimen RATHER THAN twice daily mixed insulin regimen
42
what are the types of long acting insulin given once or twice daily
for twice: insulin detemir for once: glargine and detemir once
43
type of short acting/. bolus insulin
inject insulin ANALOGUE instead of soluble human or animal or smth
44
what is Addisons disease
its autoimmune destruction of the adrenals causing primary hypoadrenalism and is the most common type of hypoadrenalism
45
addisons disease presentation- symptoms and blood findings
hyperpigmentation, weigh loss, lethargy, hyponatraemia, hypotension, hyperkalaemia, LOSS OF PUBIC HAIR in women HYPOGLYCAEMIA metabolic acidosis adrenal crisis!!!
46
common features of adrenal crisis
happens in addisons- so in hypoadrenalism shock pyrexia collapse
47
what can trigger adrenal crisis
basically when you dont have enough cortisol for your bodys demand so that can either be from increased demand aka illness or when you miss a dose of glucocorticoid aka hydrocortisone (medication= synthetic glucocort)
48
what is the medical management of addisons disease?
glucocorticoid replacement (cortisol)= hydrocortisone and mineralocorticoid replacement (aldosterone) = fludrocortisone
49
which of the two medications treating addisons is most important not to miss and replace during illness
hydrocortisone - aka glucocorticoid replacement- double dose during illness
50
other important management steps for addisons
wear a medic alert bracelet educating patients about sick day rules
51
diagnostic investigations in addisons
short synachthen test - measure cortisol before and 30 minutes!! after giving 250ug IM.
52
what is another thing you can test for that confirms addisons disease
adrenal autoantibodies such as 21 hydroxylase
53
what investigation can be done if short synacthen test is not available eg in primary care environment and result interpretation
9 am serum cortisol can be useful: > 500 nmol/l makes Addison's very unlikely < 100 nmol/l is definitely abnormal 100-500 nmol/l should prompt a ACTH stimulation test to be performed
54
cushings syndrome categorise causes including which is the most common one
cushings syndrome means hyperadrenalism causes are: exogenous (most common - aka taking steroids) endogenous- further devided to ACTH dependent and independent dependent means ACTH is high causing high cortisol ect either: -ectopic from malignancy (eg small cell lung cancer) - due to pituitary adenoma ect - (aka cushings DISEASE) -- way more common INDEPENDENT means the ACTH is low trying to lower adrenal hormones but problem is in adrenals= most commonly: adrenal adenoma
55
presentation of cushings syndrome
weight gain, buffalo bump, hirsuitism, poor glycaemic control, hypernatraemia, hypokalaemia!!!!!, metabolic alkalosis!
56
what is pseudo-cushings
mimics Cushing's often due to alcohol excess or severe depression causes false positive dexamethasone suppression test or 24 hr urinary free cortisol insulin stress test may be used to differentiate
57
which cause of cushings syndrome is associated with particularly pronounced hypokalaemia?
ectopic acth due to malignancy
58
most common tests used to investigate cushings?
overnight (low-dose) dexamethasone suppression test this is the most sensitive test and is now used first-line to test for Cushing's syndrome patients with Cushing's syndrome do not have their morning cortisol spike suppressed 24 hr urinary free cortisol two measurements are required bedtime salivary cortisol two measurements are required
59
Cushing's syndrome due to other causes (e.g. adrenal adenomas) dexamethasone suppression test findings
cortisol not supressed acth supressed
60
61
Cushing's disease (i.e. pituitary adenoma → ACTH secretion) dexamethasone suppression test findings
cortisol suppressed acth suppressed
62
Ectopic ACTH syndrome dexamethasone suppression test findings
cortisol Not suppressed acth Not suppressed
63
whaT THING does the dexamethasone supression test basically suppress
basically it supresses corticotrophs in pituitary so acth releasing cells so if youre hyperadrenal due to that you are totally supressed by test vs if its adrenal cause only acth suppressed vs if ectopic nothing supressed
64
Cushing's and pseudo-Cushing's differentiating test
insulin stress test
65
CRH stimulation is another test used to investigate cushings syndrome. what does it tell us
if pituitary source then cortisol rises if ectopic/adrenal then no change in cortisol
66
MANAGEMENT OF cushings syndrome
depends on the cause, so for ex if afrenal adenoma you remove, if malignancy ect different management for each!
67
what is the method of measuring BP appropriate for diagnosis of Hypertension?
ABPM ambulatory blood pressure monitoring or HBPM home blood pressure monitorning: you manually take bp twice daily for 4-7 days 2 recordings 1 min apart per time and use lowest one + discard all the first day measurements
68
what are the grades of hypertension (without values just name them)
grade 1 grade 2 severe
69
BP values that are considered hypertension stage 1 in clinic and at home
home: > 135/85 (in ABPM Or HBPM) clinic: > 140/ 90
70
BP values for hypertension stage 2
home> 150/95 or clinic 160/ 100
71
severe hypertension BP values
EITHER systolic > 180 OR diastolic > 120
72
who gets ACEi or ARB as first line anithypertensive management?
< 55 OR diabetic of any age
73
when does soemone get the ARB insteade of ACEi ?
when ACEi contraindicated due to cough
74
which groups DO NOT get ACEi or ARB as first line and what do they get?
black and > 55s get CLACIUM CHANNEL BLOCKER!!! (amlodipine ect)
75
what are the combinations if hypertension is not controlled on 1 drug
A+ C OR A+D ( d being thiazide like diuretic)
76
after what age is there a higher Ht BP TARGET?
after 80 its 150/ 90 in clinic and 145/ 85 at home
77
what mineral imbalance can be brought on by antihypertensive medications?
hyperkalaemia: ACE INHIBITORS, ARB hypokalaemia: thiazide like diuretics,
78
most common cause of secondary hypertension and other causes
primary hyperaldosteronism other causes are renal impariment and endo causes and drugs, preg, coarctation of aorta
79
What is diabetes insipidus
its when there is a deficiency in the hormone ADH (or arginine vasopressin) and there is cranial (central) and nephrogenic diabetes insipidus
80
symptoms of diabetes insipidus
polydipsia polyuria
81
diabetes insipidus investigations (general diagnosis not type)
high plasma osmolality (often >295 mOsm/kg), low urine osmolality (often <300 mOsm/kg) a urine osmolality of >700 mOsm/kg generally excludes diabetes insipidus water deprivation test
82
diabetes insipidus type determination
a desmopressin test can help differentiate cranial from nephrogenic DI (an increase in urine osmolality suggests cranial DI)
83
management of cranial diabetes insipidus
desmopressin
84
management of nephrogenic diabetes insipidus
THIAZIDES and low SALT AND PROTEIN diet!!!
85
why do you get hypercalcaemia in malignancy (mechanism)
Malignancy: the commonest cause in hospitalised patients. PTHrP from the tumour e.g. squamous cell lung cancer bone metastases myeloma,: due primarily to increased osteoclastic bone resorption caused by local cytokines (e.g. IL-1, tumour necrosis factor) released by the myeloma cells
86
what is the main investigation in hypercalcaemia?
measuring parathyroid hormone levels is the key investigation for patients with hypercalcaemia
87
features of hypercalcaemia?
bones, stones, groans and psychic moans corneal calcification shortened QT interval on ECG hypertension
88
initial management of hypercalcaemia
rehydrate with normal saline
89
next steps of management in hypercalcaemia
bisphosphonates may be used. They typically take 2-3 days to work with maximal effect being seen at 7 days Other options include: calcitonin - quicker effect than bisphosphonates steroids in sarcoidosis Loop diuretics such as furosemide are sometimes used particularly in patients who cannot tolerate aggressive fluid rehydration. - caution - may worsen electrolyte derangement and volume depletion.
90
other causes of hypercalcaemia including most common one
primary hyperparathyroidism (malignancy is most common in hospitalised) sarcoidosis other causes of granulomas may lead to hypercalcaemia e.g. tuberculosis and histoplasmosis vitamin D intoxication acromegaly thyrotoxicosis
91
causes of hypothyroidism
primary and secondary primary 1) in developed countries most commonly is Hashimotos 2) in developing: dietary iodine deficiency thyroid gland damage 3)- overtreatment of hyperthyroidism secodnary: pituitary tumour PRESSING on the anterior pituitary and disabling the release of TSH BRAIN TRAUMA
92
what is the pathophysiology of hashimotos thyroiditis
its an autoimmune condiitons where various autoantibodies (ex. anti-TPO, ) Attack various aspects of the follicular cells in the thyroid leading to damage of the gland, eventually disabling it from producing thyroid hormones.
93
what is the explanation behind a potential phase of hyperthyroidism in hashimotos thyroiditis
destruction of follicular cells leads to the release of thyroid hormones pre made and stored inside them since the cell bursts open. leading to a small wave of hyperthyroidism
94
symptoms of hypothyroidism
all the consequences of a low metabolism: general: weight gain, fatigue, feeling cold, insomnia, bradycardia, dry skin, nails falling off, brittle hair, myxedema: swollen tongue, face ect
95
what is the mechanism behind myxedema in hypothyroidism?
myxedema means: myxa + oedema= non pitting oedema literally caused by thick mucus like substance under skin in soft tissues its caused by the increased TSH and TRH stimulating fibroblasts in soft tissues to produce glycosaminoglycans - deposit in interstitial space causing this oedema
96
management of hypothyroidism
levothyroxine
97
levothyroxine normal dose
50-100mcg od
98
which patients need to start on a lower dose of levothyroxine and be titrated up?
patients with cardiac disease, severe hypothyroidism or patients over 50 years the initial starting dose should be 25mcg od with dose slowly titrated.
99
which hormone needs to be targeted in hypothyroidism treatment with levothyroxine
TSH! target is 0.5-2.5 mU/l i
100
how long after a change in thyroxine dose should thyroid function tests be done to monitor
after 8-12 weeks
101
what shoud be done for women with hypothyroidism who get pregnant
have their dose increased by at least 25-50 micrograms levothyroxine due to the increased demands of pregnancy. The TSH should be monitored carefully, aiming for a low-normal value
102
side effects of levothyroxine therapy
hyperthyroidism: due to over treatment reduced bone mineral density worsening of angina atrial fibrillation
103
what other medicaitons/ treatments can lecvpthyroxine therapy interact with, what is the interaction and what should be done to avoid?
iron, calcium carbonate absorption of levothyroxine reduced, give at least 4 hours apart
104
what is a life threatening complication of hypothyroidism
myxedema comma - SEVERE hypothyroidism affecting the brian causing drowsyness and brainfog and leading to comma and if untreated - death
105
thyrotoxicosis vs hyperthyroidism?
Hyperthyroidism = thyroid working too much. Thyrotoxicosis = too much thyroid hormone in blood, no matter where it comes from. All hyperthyroidism causes thyrotoxicosis, but not all thyrotoxicosis is due to hyperthyroidism.
106
causes of thyrotoxicosis
1) Graves thyroiditis 2) overtreatment for hypothyroidism 3) toxic nodular gioter 4) toxic multinodular goiter secondary: pituitary tumours SECRETING TSH
107
what other symptoms may someone with thyrotoxicosis due to a pituitary tumour have?
increased prolactin so nipple discharge or period stop
108
pathophysiology of Graves thyroiditis
autoantibodies to TSHr that SIMMULATE tsh sto they STIMULATE the receptor leading to excess thyroid hormone production. this leads to low TSH levels from pituitary. thyroid swells up and theres a smooth goiter
109
symptoms of graves
weight loss despite increased appetite and intake, heat intolerance, stress, diarrhoea, tachycardia,
110
what disease gives you pretibial myxedema
graves disease
111
pathophysiology of pretibial myxedema
TSHr antibodies stimulate fibroblasts in soft tissue but specifically surorunding the tibia to produce glycosaminoglycans that dpeosit in the interstitial space leading to myxedema
112
what is a severe life threatening complication of graves
thyroid storm - when you skip a dose or body under stress ege surgery illness ect and thyroid hormones are too high leading to tachycardia potentially turning to arrhytmia and heat intolerance to fever ect and can die
113
management of thyroid storm
symptomatic treatment e.g. paracetamol treatment of underlying precipitating event beta-blockers: typically IV propranolol anti-thyroid drugs: e.g. methimazole or propylthiouracil Lugol's iodine dexamethasone - e.g. 4mg IV qds - blocks the conversion of T4 to T3
114
what is the initial management of graves disease
beta blockers eg propanolol to control symptoms (eg cardiac)
115
what are the treatment options for graves disease and which is most commonly used now and why
1) anti thyroid drugs (ATD)-- preferred recently bc good at QUICKLY controlling hyperthyroid symptoms and protective in HIGH risk groups eg cardiac history and older patients + less side effects compared to block and replace 2) block and replace regime 3) radioiodine therapy
116
example of Anti thyroid drug
carbimazole
117
how long does anti thyroid therapy last and describe the progression + biggest complication
12-18 months start at 40 mg dose of carbimazole and reduce gradually to maintain euthyroidism VERY SERIOUS AND IMPORTANT: agranulocytosis is biggest complication (severe drop in neuts= high risk of life threatening infection- any sign of illness is red flag!!!)
118
describe block and replace therapy (duration and proccess)
carbimazole is started at 40mg thyroxine is added when the patient is euthyroid treatment typically lasts for 6-9 months
119
who is radioiodine therapy used in?
often used in patients who relapse following ATD therapy or are resistant to primary ATD treatment
120
contraindications to radioiodine therapy
contraindications include pregnancy (should be avoided for 4-6 months following treatment) and age < 16 years. Thyroid eye disease is a relative contraindication, as it may worsen the condition
121
what proportion of patients become hypothyroid?
depends on the dose given, but as a rule the majority of patient will require thyroxine supplementation after 5 years
122
symptomatic triad of graves disease
eye disease dermopathy hyperthyroidism
123
trauma where causes hyper and hypothyroidism respectively
in thryoid: hyperthyroidism due to swelling up of the thyroid and brain= pituitary- causes hypothyroidism due to low TSH secretion
124
what is the vitamin d like in secondary and tertiary and primary hyperparathyroidism
low in secondary since it is often the cause of low calcium (As vit d helps absorb calcium) and in tertiary can be low or maybe it h`s normalised priamry has nothing to do with low vit d theoretically but if they coexist randomly can be confusing
125
DKA resolution definition
ph> 7.3 ketones <0.6 bicarb > 15

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