endo conditions Flashcards
1
Q
what type of disorder is T1 diabetes
A
autoimmune disorder
2
Q
which cells are destroyed in T1 diabetes
A
B cells of pancreas
3
Q
describe the pathology of T1 diabetes
A
T-cell mediated destruction of pancreatic Beta cells= no insulin production
cells cannot uptake glucose without insulin- body thinks its fasting, alpha cells releaes glucagon to increase blood glucose = hyperglycaemia
4
Q
what are the responses of alpha and beta cells of the pancreas to high vs low blood glucose levels
A
low blood glucose > detected by alpha cells = they secrete glucagon
(glucagon breaks down glycogen to release glucose from liver + musc cells)
high blood glucose > detected by beta cells= they secrete insulin
(insulin helps liver + muses take up more glucose and convert it to glycogen)
5
Q
how does T1 diabetes present
A
@childhood
polyuria, polydipsia, sudden weight loss
6
Q
requirements for T1 diagnosis
A
symptom patient= raised plasma glucose levels detected once
asymptomatic patient= raised plasma glucose levels detected x2
7
Q
what are the plasma glucose levels required for a T1 diagnosis
A
fasting= over 7mmol/L
random= over 11.1mmol/L
oral-
fasting= over 7mmol/L
2hrs after glucose= over 11.1
8
Q
treatment for T1
A
diet monitoring
basal and bolus insulin
9
Q
what happens in ketoacidosis
A
not enough glucose, therefore liver breaks down fats into ketones for energy
10
Q
what levels does a diabetic ketoacidosis diagnosis require
A
hyperglycaemia- over 11.1mmol/L
ketosis- over 3 mmol/L
acidosis- pH lower than 7.3
11
Q
causes of diabetic ketoacidosis
A
infection,
untreated DM
myocardial infarction
12
Q
symptoms of ketoacidosis
A
nausea/vomiting, pear drop breath, drowsy and confused, dehydration therefore hypotension, polyuria, polydipsia, glycosuria, hyperventilation
13
Q
tests for DKA
A
measure blood glucose and blood gas- resp comp
U& E
urine dipstick
14
Q
treatment for DKA
A
ABC management
replace fluids with 0.9% saline
give glucose + insulin @ same time to prevent hypoglycaemia
15
Q
what is a complication of insulin treatment
A
-causes raised K+/Na+ activity
therefore can cause hypokalaemia
16
Q
pathology of T2 diabetes
A
repeated exposure to high levels of glucose- B cells become fatigued/ cells become resistant to insulin and take up less glucose
= chronic hyperglycaemia
17
Q
how does T2 present
A
polyuria, polydipsia, polyphagia, polyglycosuria
18
Q
what is done to test for T2
A
best= HbA1c test- tells average blood glucose level for last 3 months
diagnosis = over 48 mol/L
prediabetes diagnosis= 42-47 mmol/l
- can also use same blood glucose tests as T1
19
Q
treatment of T2 (4 lines)
A
1st- lifestyle modifications
2nd- metformin, increases insulin sensitivity, decreases hepatic gluconeogenesis
3rd- add a sulfonylurea, pioglitazone, DPP-4 inhibitor or SGLT-2 inhibitor.
4th- insulin
20
Q
what doesn’t occur in hyperosmolar hyperglycaemic state
A
no acidosis/ketosis
21
Q
what is the level of osmolality above in hypersomolar hyperglycaemic state
A
above 320 mosmol/Kg
22
Q
treatments for hyperosmolar hyperglycaemic state
A
fluid replace- iv 0.9% saline
VTE prophylaxis
anticoagulants for dehydration- enoxaporin
last resort= insulin
23
Q
what is glucose concentration below in hypoglycaemia
A
normal fasting level= aka below 3 mmol/L
24
Q
what is the normal response to hypoglycaemia
A
drop in blood glucose levels = norepinephrine & acetylcholine stimulates alpha islet cells 2 produce glucagon
stimulates production of adrenaline, GH , cortisol
inhibits insulin production
blood glucose increases
25
what are the autonomic and neuroglycopenic blood glucose concentrations in hypoglycaemia
autonomic= less than 3.3
neuroglycopenic= less than 2.8
26
describe whipple's triad for hypoglycaemia
whipple's triad
-signs and symptoms
-low blood glucose (less than 3)
-resolution of symptoms with correction of blood glucose
27
treatment for hypoglycaemia
community- IM/SC syringe of glucagon, oral glucose 10-20g
hospital- alert= quick acting carb
unconscious= SC/IM glucagon
or IV 20% glucose solution
28
define hypothyroidism
deficiency of thyroid hormones, slowing down of metabolic processes
29
what is the most common type of hypothyroidism
Hashimoto's thyroiditis- primary hypothyroidism
30
what is the cause of secondary hypothyroidism
pituitary failure- not enough TSH
31
pathology of primary hypothyroidism
-T3/T4 not produced , therefore compensation = inc. production of TSH
32
pathology of secondary hypothyroidism
pituitary failure- TSH levels decrease
therefore- T3/T4 levels decrease
33
presentation of hypothyroidism
weight gain, lethargy, constipation, loss of lateral aspect of eyebrow, dry scalp, menorrhagia, cold intolerance
34
investigations for hypothyroidism
1st= TFTs- low T4 levels
antithyroid peroxidase antibodies elevated (Hashimoto's)
35
hypothyroidism treatment
levothyroxine
36
pathology of Hashimoto's thyroiditis
autoimmune formation of anti-thyroid peroxidase antibodies (anti TPO) + antithyroglobulin antibodies
- these bind to + block TSH receptors in thyroid= inadequate T4 production + high levels of TSH
- progressive fibrosis + thyroid follicles destroyed
37
define hyperthyroidism
increased synthesis of T3/T4 @ thyroid gland- therefore low levels of TSH
38
causes of hyperthyroidism
Graves disease (mc)
toxic multinodular goitre (nodules secrete thyroid hormones)
iodine excess
thyroiditis (De Quervain’s, post-partum, drug induced - iodine, amiodarone, lithium)
toxic adenoma
ectopic thyroid tissue
thyroid storm/thyrotoxic crisis
39
hyperthyroidism presentation
weight loss
heat intolerance
sweating
diarrhoea
anxiety
tremor
pretibital myxoedema
40
investigations for hyperthyroidism
TFTs- elevated T4, low TSH
41
treatment for hyperthyroidism
tremor- propranolol
2 decrease T4 levels- propylthiouracil then carbimazole (CI in preggo)
iodine radioactive treatment
surgery
42
what is the most common type of hyperthyroidism
Grave's
43
pathology of Grave's hyperthyroidism
IgG autoantibodies against TSH receptor= bind + activate receptor, causing excessive production of T3/T4
44
what are presentations unique to Grave's
diffuse goitre, digital clubbing
45
define De Quervain's thyroiditis
inflammation of thyroid gland caused by viral infection
46
what are the four phases of de Quervain's thyroiditis
1-m3-6 weeks hyperthyroidism
2- 1-3 weeks, euthyroid
3- weeks 2 months= hypothyroidism
4- thyroid structure and function returns to normal
47
presentation of de Quervain's thyroiditits
enlarged thyroid, neck pain, trouble eating, fever
48
what will be elevated in De Quervain's thyroiditis
ESR and CRP
49
treatment of de quervain's thyroiditis
hyper phase, NSAIDs & corticosteroids 4 pain
hypo phase= usually no treat, if severe small dose of levothyroxine
50
name 4 types of thyroid cancer from least to most severe
papillary
follicular
medullary
anaplastic
51
which gender is more at risk of thyroid cancers
female
52
presentation of thyroid cancer
palpable thyroid nodule
53
investigations for thyroid cancer
- neck ultrasound
- laryngoscopy
- fine needle biopsy
54
treatment of thyroid cancer
thyroidectomy
radioactive iodine ablation
TSH suppression
55
what is a risk of total thyroidectomy
recurrent laryngeal nerve damage
56
define thyroid storm
tissues exposed to high levels of TSH and T4- therefore severe thyrotoxicosis
- it is a result of untreated hyperthyroidism
57
treatment for thyroid storm
1st carbimazole
2nd thyroidectomy
58
name 3 pituitary adenomas
cushing's
acromegaly
prolactinoma
59
define Cushing's
chronic abnormal elevation of cortisol
60
what is the normal feedback loop for low cortisol
negative feedback loop
low blood cortisol= CRH released from hypothalamus
stimulates pituitary to produce ACTH
stimulates adrenal glands to produce cortisol
sufficient cortisol levels = neg feedback , therefore less ACTH production
ACTH released in diurnal rhythm
61
what causes ACTH independent cushings
-oral steroids
-adrenal adenoma
62
what causes ACTH (adrenocorticotropic hormone) dependent cushings
-anterior pituitary adenoma
-ectopic ACTH production
63
presentation of cushings
moon face
buffalo hump
proximal limb wasting- proteolysis
abdo. striae
mood changes
central obesity
amenorrhea
acne
hirsutism
64
what investigations are there for cushings
1st - dexamethasone suppression test (1mg) for raised plasma cortisol
other =
24hr urinary free cortisol
chest CT- small cell lung cancer
abdo CT- adrenal adenoma
MRI brain - pituitary adenoma
65
describe the dexamethasone suppression test
dexamethasone acts as glucocorticoid
- this triggers neg feedback loop and cortisol levels will drop
1mg is given @11pm - cortisol levels measured @8am
normal- suppressed, cortisol less than 50nnomol/L
cushings- not suppressed
66
treatments for cushings
stop steroids
adrenal adenoma- adrenalectomy
pituitary adenoma- trans sphenoidal surgery
ectopic ACTH- remove neoplasm if not metatised, otherwise adrenalectomy and give replacement steroids for life
67
complications of cushings
hypertension, osteoporosis, diabetes, cardiovascular disease
68
define acromegaly
excessive secretion of growth hormone
69
what causes acromegaly
anterior pituitary adenoma- unregulated GH production
70
pathology of acromegaly
norm- GnRH released from hypo, stimulates release of GH from anterior pituitary
- excessive GH = increased levels of IGF-1
this stimulates bone and soft tissue growth
71
presentation of acromegaly
bi-temporal hemianopia
spade like hands and feet
acroparatheisa
arthralgia
bacne
oily skin
sweating
headaches
amenorrhea
mood disturbances
frontal bossing
72
investigations for acromegaly
- test for high IGF-1 levels
-MRI for adenoma
-oral glucose tolerance test
look at clinical signs
73
lines of treatment for acromegaly
1st- anterior pituitary adenoma, trans sphenoidal surgery
2nd- somatostatin analogues, block GH release
3rd pegvisomant, GH antagonist
dopamine antagonists, block GH releaase
74
complications of acromegaly
heart disease, type 2 diabetes, hypertension, arthritis, carpal tunnel
75
what is a prolactinoma
benign lactroph adenomas
-lactrophs are @ anterior pituitary, produce prolactin- stimulates breasts to produce milk
76
who is more at risk of a prolactinoma
women of child bearing age 20-40 years
77
pathology of a prolactinoma
increased prolactin levels- inhibits production of GnRH= 2ndary hypogonadism (little to no sex hormones)
78
presentation of prolactinoma female
amenorrhea
oligomenorrhea
infertility
galactorrhea
low libido
79
presentation of prolactinoma male
low testosterone
low libido
erectile dysfunction
decreased facial hair
80
investigations for prolactinoma
1st- test for elevated prolactin serum levels
2nd MRI for pituitary adenoma
81
treatment of prolactinoma
1st dopamine agonists (inhibit prolactin)
eg cabergoline, bromocriptine
2nd hormone replacement surgery
82
complications of prolactinomas
infertility, weight loss, raised inter cranial pressure due to adenoma
83
what is conn's disease
type of primary hyperaldosteronism- caused by adrenal adenoma
84
what is the pathology of conns
norm= RAAS
conns- excess aldosterone, acts on distal tubule- increased Na reabsorption, H20 retention, K excretion
85
presentation of conns
often asymptomatic
resistant hypertension, headaches, hypokalaemia, excessive thirst
86
investigations for conns
test adosterone/renin ratio (elevated =primary)
gold= fludocortisone suppression test/ IV 0.9% saline infusion testing-
conns will have failure to suppress aldosterone
can also take FBC/ U&Es/LFT
CT/MRI to locate adrenal lesions
87
treatment for conns
aldosterone antagonists 2 control BP & increase K
eg eplerenone, spironolactone
adrenalectomy
percutaneous renal artery angioplasty
88
define adrenal insufficiency
adrenal glands don't produce enough steroid hormone- esp cortisol and aldosterone
89
what type of adrenal insufficiency is addison's
primary
90
pathology of primary adrenal insufficiency
autoimmune destruction of adrenal cortex- therefore reduced steroid hormone release, ACTH no longer inhibited therefore levels increase
ACTH causes melanocytes to produce melanin- hyperpigmentation
91
pathology of secondary adrenal insufficiency
damaged pituitary- HPA axis suppression, therefore decreased ACTH from pituitary
adrenal gland not stimulated to produce cortisol- low levels of ACTH= no hyperpigmentation
92
pathology of tertiary adrenal insufficiency
inadequate CRH release from hypothalamus due to long term steroids
93
presentation of adrenal insufficiency
addison's/primary only- hyper pigmented palmar crease
gen= fatigue, weight loss, nausea, hypotension, pubic hair loss in women
94
investigations for adrenal insufficiency
short syncathen test- give synthetic ACTH
norm- cortisol levels double from baseline
primary AI- cortisol levels fail to rise (will be less than 500 nanomol/L
can also measure Na- will be lower due to decreased aldosterone
k= higher due to low aldosterone
95
treatment for adrenal insufficiency
hydrocortisone 2 replace cortisol
fludrocortisone 2 replace aldosterone
96
complication of adrenal insufficiency
adrenal crisis
97
what does SIADH stand for
syndrome of inappropriate secretion of ADH
98
causes of SIADH
idiopathic
post-op major surgery
infection
head injury
meds
malignancy
meningitis
rf= over 50
99
pathology of SIADH
increased ADH= increased h20 reabsorption- dilutes Na causing hyponatraemia
and increase in urine conc
100
presentation of SIADH
hyponatremia symptoms
-headache
-confusion
-muscle cramps
-swelling
-oedema
-dry mucous membranes
-poor skin turgor
severe= seizures + reduced consciousness
101
investigations for SIADH
diagnosis of exclusion
clinical exam= euvolaemia
U&Es = hyponatraemia
serum osmolality- decreased
102
treatment for SIADH
stop meds if causing SIADH
restrict fluid to 500mls
chronic- use vasopressin receptor anatagonists- tolraptan
103
complications of SIADH
central pontine myelinolysis due to rapid correction
104
what are the 2 types of diabetes insipidus
cranial & nephrogenic
105
what is cranial DI characterised by
decreased ADH secretion (more common)
106
what is nephrogenic DI characterised by
ADH insensitivity
107
cranial DI and its causes
hypo does not produce ADH
-idiopathic
-brain tumours
-head injury
-brain infection
-brain surgery/radiotherapy
108
nephrogenic DI and its causes
kidney collecting ducts don't respond to ADH
-inherited
-drugs (lithium)
-systemic disease
-electrolyte disturbance
109
pathology of DI
decreased ADH/ ADH insensitivity- impaired H20 retention
increased vol of dilute urine
110
presentation of DI
polyuria
polydipsia
dehydration
hypernatraemia
postural hypotension
111
investigations for DI
H20 deprivation test
urine osmolality= low
serum osmolality= high
serum glucose= used to exclude diabetes mellitus- no glycosuria
serum Na= high
24hr urine collection= greater than 3L/24hr
112
treatment for cranial DI
synthetic ADH- desmopressin
113
treatment for nephrogenic DI
thiazide diuretics- oral bendroflurethiazide
114
complications of DI
severe hypernatraemia
thrombosis
bladder & renal dysfunction
115
define hyperparathyroidism
excessive secretion of parathyroid hormone- PTH
116
what secrete PTH and what is its effect
chief cells secrete PTH 2 increase blood Ca via increased:
osteoclast activity- increased bone resorption
intestinal absorption
reabsorption from kidneys
vit D activity
117
pathology of primary hyperparathyroidism
tumour/hyperplasia of thyroid glands- xtra secretary tissue= increased PTH released
therefore hypercalcaemia
118
pathology of secondary hyperparathyroidism
insufficient vit D/ chronic renal failure= decreased Ca absorption, therefore hypocalcaemia
so parathyroid produces more PTH + hyperplasia occurs
119
pathology of tertiary hyperparathyroidism
after secondary
- glands become autonomous + don't respond to neg feedback
120
investigations for hyperparathyroidism
1st: measure serum Ca
1=high
2=low
3=high
serum phosphate-
1=low
2+3=high
can also investigate:
bones- DEXA scan, osteoporosis
stones- kidney stones
groans- abdo x-ray
adenomas- radioisotopic scanning
121
treatments for hyperparathyroidism
primary- remove tumour
secondary- vit D replacement/kidney transplant
tertiary- parathyroidectomy
122
define hypocalcemia
low serum calcium=
<8.5mg/dL, < 2.20 mmol/L
123
causes of hypocalcemia
post parathyroid surgery- hyperparathyroidism
vit D deficiency
hyperventilation
drugs
malignancy
toxic shock
124
how does hypocalcemia present
CATS go numb
C onvulsions
A rrhythmias
T etany
S pasms and stridor
numbness in the fingers
125
investigations for hypocalcemia
lab tests 4 levels of PTH, vit D albumin, phosphorus, magnesium
check if Ca= <8.5mg/dL
ECG- prolonged QT interval
126
treatment for hypocalcemia
severe= IV Ca- 10ml of 10% over 10mins
gluconate
persistant= vit D supplements
127
define hypercalcemia
serum Ca= > 12mg/dL
increased PTH= increased Ca
128
what causes hypercalcemia
hyperparathyroidism
malignancy
sarcoidosis
thyrotoxicosis
drugs
129
presentation of hypercalcemia
painful bones
renal stones
abdo groans
psych moans
short QT interval
130
investigations for hypercalcemia
fasting serum Ca + phosphate samples
serum PTH & Ca levels=elevated
ultrasound
131
treatment for hypercalcemia
rehydrate with norm saline then bisphosphonates
loop diuretics eg furosemide
132
what is hypokalemia
serum K level < 3.5mmol/L
133
causes of hypokalemia
reduced potassium intake
increased K entry into cells
increased K excretion
Mg depletion
hyperaldosteronism
can happen with alkalosis or acidosis
134
presentation of hypokalemia
musc weakness
hyporeflexia
cramps
tetany
palpitations
light headedness
arrythmias
constipation
abnormal ECG
135
investigations for hypokalemia
metabolic panel
ECG
U&Es
136
treatment for hypokalemia
mild (3-3.4mmol/L)= oral replacement, maybe IV
severe= <2.5mmol/L - give IV potassium chloride
137
complications of hypokalemia
cardio=
chronic heart failure
acute MI
arrhythmia
muscle=
weakness
depression of deep tendon reflexes
rhabdomyolysis
138
define hyperkalemia
serum potassium = >5.5mmmol/L
139
causes of hyperkalemia
increased K uptake
increased K production
redistribution- shifts from intra to extracellular
decreased Na production
140
presentation of hyperkalemia
must weakness + paralysis
fasat & irregular pulse
chest pain
light headiness
ECG:
-tall and tented T wave
-small p waves
-wide QRS complex
141
investigations for hyperkalemia
metabolic panel (CMP)
ECG
U&Es
142
treatment for hyperkalemia
ECG changes- IV ca gluconate/chloride (won't lower k levels)
if no ECG changes- shift k into cells via combined insulin/dextrose infusion
nebulised salbutamol
remove K from body via Ca resonium, loop diuretics, dialysis
can also stop excacerbating drugs, eg ACE inhibitors + treat underlying cause
143
define carcinoid syndrome
carcinoid tumour releases serotonin + other vasoactive peptides into systemic circulation
144
cause of carcinoid syndrome
| where do they occur most often
caused by a neuroendocrine tumour that secretes serotonin + other chemicals into blood stream
most common 2 least common
GI
lungs
liver
ovaries
thymus
small intestine malignancy- most common @ appendix
liver= most common 4 metastasis
145
presentation of carcinoid syndrome
flushing
diarrhoea
abdo cramps
bronchospasm
fibrosis
palpitations
146
investigations for carcinoid syndrome
urinary 5-Hydroxyindoleacetic Acid test- levels= elevated
MRI/CT of chest+pelvis 2 locate tumours
147
treatment for carcinoid syndrome
surgery
somatostatin analogues eg octreotide
148
define hypernatremia
serum Na conc= >145mmol/L
149
causes of hypernatremia
dehydration/fluid restriction
excessive water loss-diuretics
diabetes insipidus
conn's or cushing's
150
pathology of hypernatremia
net water loss/ excessive Na intake
serum sodium increases, the plasma osmolality increases, which triggers the thirst response and ADH secretion, leading to renal water conservation and concentrated urine
151
presentation of hypernatremia
can be asymptomatic
thirst
weakness
lethargy
irritability
confusion
seizures+ coma
152
investigations for hypernatremia
1st= metabolic panel
serum Na- elevated
other= venous blood gas, u&Es, serum osmolality (high)
153
treatment for hypernatremia
fluid replacement and correct serum Na
(can cause cerebral oedema if fluid given too quick)
154
define hyponatremia
serum Na= <135mmol/L
155
causes of hyponatremia
GI fluid loss via vomit/diarrhoea
fluid overload
mineral corticoid deficiency
diuretics
156
pathology of hyponatremia
decreased serum Na= decreased plasma osmolality, therefore fluid shifts intracellularly- causes swelling + oedema
157
presentation of hyponatremia
can be asymptomatic
reduced consciousness
swelling/oedema
dry mucous membranes
poor skin turgor
headache
confusion
malaise
158
investigations for hyponatremia
metabolic panel- serum Na= decreased
other= U&Es + serum osmolality (low)
159
treatment for hyponatremia
symptomatic= hyperatonic saline infusion
asymptomatic= fluid restriction, isotonic fluid infusion
160
define phaeochromocytoma
rare catecholamine-producing tumour of chromaffin cells in adrenal medulla
161
risk factor for phaeochromocytoma
162
causes of phaeochromocytoma
inherited (eg, MEN-2)
idiopathic
neurobromatosis
von hippel Lindau disease
163
pathology of phaeochromocytoma
adrenaline produced by chromaffin cell @adrenal medulla- phaeochromocytoma secretes excessive catecholamines (adrenaline + noradrenaline)- stimulates SNS & flight/fight response
164
presentation of phaeochromocytoma
episodic headache
sweating and tachycardia
palpitations
tremor
hypertension
retinopathy
impaired glucose tolerance
165
166
treatment for phaeochromocytoma
hypertensive crisis= antihypertensive agents eg phentolamine
no hypertensive crisis= alpha blocker eg phenoxybenzamine
beta blocker eg atenolol/propanolol
adrenalectomy if possible
monitor BP + plasma metanephrines
