5. ENDOCRINOLOGY Flashcards
1
Q
what type of disease is type 1 diabetes mellitus, what does it cause destruction of and what is the consequence of this (3)
A
autoimmune disease
causes destruction of beta cells in pancreas
causes absolute insulin deficiency
2
Q
what type of reaction is T1DM
A
type 4 hypersensitivity
3
Q
what are the causes of T1DM 2
A
combination of genetics and environmental triggers
4
Q
what are the consequences of the body not making insulin in T1DM (4 steps), start with body being unable to produce insulin to digest carbohydrates
A
cells cannot take in glucose
the body thinks it is being fasted
gluconeogenesis occurs in liver
causing more hyperglycaemia
5
Q
when does T1DM usually manifest and what does it present in the form of
A
in childhood
diabetes ketoacidosis
6
Q
what are 4 symptoms of T1DM
A
polyuria, polydipsia, glucosuria, sudden weight loss
7
Q
explain polyuria in diabetes 1 reason only
A
glucose excretion in urine draws water with it because glucose is osmotically active
8
Q
what is the max reabsorption value for glucose in the kidneys
A
10mmol/L
9
Q
explain sudden weight loss in T1DM
A
due to breakdown of adipose and muscle tissue as an alternative energy source to glucose
10
Q
explain polydipsia in diabetes
A
extreme thirst due to fluid loss via urine
11
Q
what is required for a diagnosis of T1DM 2
A
one abnormal glucose value and symptoms or two abnormal glucose values in asymptomatic
12
Q
what is fasting glucose value determines diabetes mellitus and units
A
> =7mmol/L
13
Q
what is fasting glucose value determines pre diabetes and units
A
> 6mmol/L
14
Q
what HbA1c value determines diabetes mellitus and units
A
> =48mmol/mol
15
Q
what HbA1c value determines pre diabetes and units
A
> 41mmol/mol
16
Q
what is the gold standard investigation test for diabetes mellitus
A
HbA1c test
17
Q
what random glucose value/ glucose tolerance test value determines diabetes mellitus and units
A
> =11.1mmol/L
18
Q
what is the GS treatment for T1DM (2)
A
combination of long lasting 12-24 hour basal insulin dose and a short acting bolus injected 30 mins before meals
19
Q
what is vital for treating T1DM patients
A
patient education- to monitor dietary glucose intake
20
Q
how long is the treatment for T1DM
A
lifelong
21
Q
what can diabetic ketoacidosis be classed as
A
a life threatening medical emergency
22
Q
what are the causes of diabetic ketoacidosis (DKA) 4
A
untreated T1DM
LOW insulin therapy
infection/ illness
myocardial infarction
23
Q
explain the pathophysiology of DKA starting with insulin deficiency
A
glucose not able to be absorbed
alternative sources of energy is to break down free fatty acids from adipose tissue
this is oxidised to acetyl coA to produce ketones
ketones are acidic and cause blood acidosis
24
Q
what is the compensation for DKA and what is this due to/ countering
A
respiratory compensation
due to metabolic acidosis
25
symptoms of DKA (3)
signs of DKA (2)
nausea, vomiting, dehydration, acetone-smelling breath, Kaussmal's breathing
26
what other symptoms does DKA present with
symptoms of DM- glucosuria, polyuria, polydipsia
27
what 3 things are required for a DKA diagnosis (not specific values)
1. symptoms
2. hyperglycaemia
3. blood gas sample showing metabolic acidosis with respiratory compensation
28
what value dictates acidosis in the blood
pH <7.3
29
what test can be done to identify ketone levels and what value is DKA
blood ketone test
>3mmol/L
30
what is treatment for DKA (4 steps)
1. ABC
2. 0.9% NaCl infusion
3. give insulin and glucose simultaneously
4. correct hypokalaemia if this occurs
31
what are the three complications of DKA treatment
1. cerebral oedema
2. hypokalaemia
3. hypoglycaemia
32
explain why hypokalaemia is a complication of DKA treatment and what effect it has on the body 1
insulin treatment for DKA causes intracellular shift of K+ which can cause muscle weakness
33
explain why hypoglycaemia is a complication of DKA treatment
insulin treatment can cause glucose levels to drop rapidly into hypoglycaemia
34
what is T2DM's insulin deficiency and how does T2 cause hyperglycaemia
relative insulin deficiency
insulin resistance in liver and muscle cells causes hyperglycaemia
35
Name 4 non modifiable and 4 modifiable risk factors for T2DM
Non: age, family history, male, ethnicity
modifiable: obesity, hypertension, sedentary lifestyle, high carb diet
36
explain the pathophysiology of T2DM starting with hyperglycaemia, including the role of the pancreas
hyperglycaemia causes increased insulin resistance in cells
pancreas compensates by producing large volumes of insulin but is damaged by overworking and toxic glucose levels
37
what are the 4 symptoms of T2DM
polyuria, polydipsia, polyphagia, glycosuria
38
how is T2DM found
picked up incidentally on routine blood tests
39
what are the diagnosis and investigations for T2DM
exactly the same as T1DM
40
what are the 4 lines of treatment for T1DM (1,1,4,1)
1st: lifestyle modifications eg lose weight
2nd: metformin
3rd: add sulfonylurea, PIOGLITAZONE, DPP-4 inhibitor or SGLT-2 inhibitor
4th: insulin
41
how does the SGLT2 inhibitor work? and name examples
inhibits reabsorption of glucose in the proximal tubule via the sodium-glucose transporter, resulting in more glucose to be excreted eg empagliflozen/ dapagliflozen
42
how does the DPP4 inhibitor work? and name an example
DPP4 inhibitor blocks DPP4 enzyme which prevents inhibition of GLP1. Overall effect= increased insulin production in response to a meal being sensed by the body (eg chewing) eg sitagliptin
43
how do sulfonylureas work and give an example
sulfonylurea binds to bind to K+ channels on beta pancreatic cells, reducing K+ efflux which causes depolarisation of the cell. There is a Ca2+ influx due to the action potential which stimulates insulin release from vesicles in the cell eg Gliciazide
44
how does metformin work
inhibits the AMPK enzyme in the liver which inhibits gluconeogensis, decreases intestinal glucose absorption and increases insulin sensitivity
45
what are the 3 microvascular complications of DM
retinopathy
peripheral neuropathy
nephropathy
46
what are the 4 macrovascular complications of DM
stroke
hypertension
peripheral artery disease
coronary artery disease
47
explain retinopathy associated with diabetes and what can this lead to
high blood pressure and glucose levels damages retina= blindness
48
explain peripheral neuropathy associated with diabetes and what can this lead to
high glucose levels damage blood vessels supplying nerves= pain/ numbness
49
explain nephropathy associated with diabetes and what can this lead to
progressive deterioration of kidney function due to damage to blood vessels and nephrons in kidney= kidney disease
50
explain stroke associated with diabetes and what can this lead to
high glucose levels damage blood vessels in brain which can lead to stroke
51
explain how diabetes can lead to development of hypertension
more likely to get atherosclerosis which can narrow blood vessels and cause hypertension
52
explain peripheral artery disease associated with diabetes
more likely to get atherosclerosis which narrows vessels that carry blood from heart to legs
53
explain coronary artery disease associated with diabetic hypertension
hypertension caused by diabetes causes increased force exerted on artery walls which can damage them
54
what can hyperosmolar hyperglycaemic state be classed as
a life threatening medical emergency
55
what are the 3 characteristics of hyperosmolar hyperglycaemic state
hyperglycaemia, hyperosmolarity, NO KETOSIS
56
who typically presents with hyperosmolar hyperglycaemic state 2
elderly with T2DM
57
explain the pathophysiology of hyperosmolar hyperglycaemic state starting with hyperglycaemia and ending with what this does to the blood
hyperglycaemia causes osmotic diuresis and the volume depletion in the body increases the serum osmolarity causing hyperviscosity of blood
58
what is osmotic diuresis and how does it cause electrolyte imbalances
increased urination in response to hyperglycaemia: excreted glucose in urine takes water with it so sodium and potassium follow the water and are excreted in the urine
59
what is the presentation of hyperosmolar hyperglycaemic state (6) 2 signs and 4 symptoms
fatigue, nausea, vomiting, dehydration, HYPOTENSION, TACHYCARDIA
60
what are the 3 haematological complications of hyperviscosity of blood and what condition does this occur in
MI, stroke, peripheral arterial thrombosis
hyperosmolar hyperglycaemic state
61
how can you diagnose hyperosmolar hyperglycaemic state (3)
1. severe hyperglycaemia (>30mmol/L)
2. hyperosmolarity (>320mosmol/kg)
3. no acidosis or ketosis
62
what is the treatment for hyperosmolar hyperglycaemic state (4)- acronym of 4 letters
1. fluid replacement with saline
2. venous thromboembolism prophylaxis eg LWMH like enoxaparin
3. give insulin if glucose levels do not decrease
4. give K+ if K+ levels aren't naturally corrected
SVIK
63
what are the two complications related to treatment of hyperosmolar hyperglycaemic state
1. insulin related hypoglycaemia (due to excessive high-dose insulin therapy)
2. treatment related hypokalaemia (due to high-side insulin therapy)
64
what is the defining value of hypoglycaemia
blood glucose levels below 3mmol/L
65
what is the body's response to low glucose levels (3:3, 2, 1)
1. increased in adrenaline, GROWTH HORMONE, cortisol
2. gluconeogensis and glyceogenolysis in liver
3. decreased insulin secretion
66
what is the pathophysiology behind why hypoglycaemia occurs
body's mechanisms to increase glucose levels are not working correctly
67
what are the two categories of causes for hypoglycaemia
diabetic causes and non-diabetic causes
68
state the 2 diabetic causes of hypoglycaemia
1. excessice levels of insulin
2. medication effect when increasing dose or starting on sulfonylureas
69
state the 6 non-diabetic causes of hypoglycaemia
exogenous medication eg aspirin overdose/
pituitary insufficiency
liver failure
alcohol
addisons
islet cell tumor
non-pancreatic neoplasm
70
what are the 4 symptoms of blood glucose <3.3mmol/L and what can these be categorised as
sweating, shaking, hunger, anxiety
autonomic
71
what are the 3 symptoms of blood glucose <2.8mmol/L and what can these be categorised as
weakness, vision changes, confusion
neuroglycopenic
72
what are the two rare and most severe symptoms of hypoglycaemia
seizures and coma
73
what does diagnosis of hypoglycaemia involve (1)
1. whipples triad (symptoms of hypo, low blood glucose, resolution of symptoms with correction of glucose levels)
74
what is a gold standard investigation for hypoglycaemia
48 to 62 hour fast with blood glucose monitoring
75
how can hypoglycaemia be treated in the community (2)
1. oral glucose
2. hypoglycaemia kit if prescribed containing vial of glucose for injection
76
how can hypoglycaemia be treated in hospital (3)
1. oral glucose if patient is alert
2. SC/IM injection of glucagon if unconscious
3. alternative is IV 20% glucose solution
77
what is hypothyroidism and what does is generally cause
thyroid hormone deficiency
generalised slowing of processes
78
what are the two types of hypothyroidism and how do they each cause hypothyroidism
primary- issue with thryoid gland, lack of T3/4 (one i in thyroid= 1)
secondary- issue with pituitary, lack of TSH (two i in pituitary= 2)
79
what are the causes of primary hypothyroidism (4)
Hashimotos thyroiditis, De Quervain's thyroiditis, dietary iodine deficiency, carbimazole
80
what is the cause of secondary hypothyroidism (1)
pituitary adenoma
81
what three diseases are associated with hypothyrodiism
downs and turners syndrome and coeliac disease (DOWN the stairs, TURN the corner and you'll SEE it)
82
6 symptoms of hypothyroidism
weight gain, lethargy, cold intolernace, loss of lateral aspect of eyebrow, constipation, fluid retention
83
what are the investigations for hypothyroidism (3)
1st line, 1 for autoimmune causes and 1 for associated condition
1st line: thyroid function test
2. antithyroid peroxidase antibody levels for autoimmune causes
3. fasting blood glucose in patients with non-specific fatigue and weight gain due to association with T1DM
84
what are the thyroid function test results for primary and secondary hypothyroidism
primary: low T3, high TSH
secondary: low T3, low TSH
85
treatment for hypothyroidism and how does this work
levothyroxine
synthetic T4
86
what is hashimotos thyroiditis, what does it lead to and what type of hypothyroidism does it cause
thyroid gland is attacked by immune system via antithyroid antibodies and leads to loss of function
primary hypothyroidism
87
what two diseases can hashimotos be associated with
T1DM
addisons
88
what is the presentation of hashimotos like 2 and what does this progress to
same as hypothyroidism
plus goitre of thyroid gland which progresses to atrophy
89
what is the gold standard investigation for hashimotos
antithyroid peroxidase antibodies test should be positive (anti-TPO)
90
what causes hyperthyroidism 1 (pathophys)
increased synthesis of T3/4 by the thyroid gland
91
what is thyrotoxicosis and what can it be classed as and how it is different from hyperthyroidism
clinical syndrome of increased thyroid hormones in circulation
hyperthyroidism= increased secretion of thyroid hormones
92
what are the two types of hyperthyroidism and explain how each causes hyperthyroidism
primary- issue with thyroid gland, too much T3/4
secondary- issue with pituitary gland- too much TSH
93
what are the causes of hyperthyroidism (4)
Graves, iodine excess in diet/ meds, De quervains thyroiditis, levothyroxine
94
symptoms of hyperthyroidism (6)
weight loss, heat intolerance, diarrhoea, increased sweating, tacchycardia, tremor
95
what are the investigations for hyperthyroidism 2 (1 is looking into autoimmune causes)
1. thyroid function test
2. anti TSH receptor antibody test
96
what is the treatment for hyperthyroidism 4) and treatment to support symptoms 1 and what type of symptoms r these
1. thionamides eg carbimazole/ prophylthiouracil
2. BETA BLOCKER eg propanalol (blocks adrenaline related symptoms)
3. radio-iodine treatment
4. surgery
97
what is graves disease and what is the effect of this
autoimmune condition where antibodies are produces to TSH receptors
increased T3/4 synthesis which increases thyroid hormones production
98
what are the values for the thyroid function test for Graves
high T3/4, low TSH
99
what are the two causes of graves disease
alemetuzumab (MS drug)
autoimmune
100
what is the pathophysiology of graves disease
thyroid stimulating immunoglobulins (TSI) are made to TSH receptor and they bind and activate the receptor causing autonomous production of thyroid hormones
101
symptoms of graves (+3)
same as hyperthyroidism plus pretibial myxoedema, exophthalmos and thyroid acropathy
102
what is pretibial myxoedema
TSH antibodies react with skin in front of tibia= waxy, discoloured appearance
103
what is exophtahlmos
peri orbital inflammation which causes eyelid retraction
104
what is thyroid acropathy (3)
triad of digital clubbing, soft tissue swelling of hands and feet, periosteal new bone formation
105
what is the treatment for graves (3+ for severe orbitopathy)
1. antithyroid drugs eg carbimazole
2. radioactive iodine therapy drink
3. surgery to remove part of thyroid gland
4. first line for severe orbitopathy is IV corticosteroid eg methyprednisolone
106
what is de quervains thyroiditis
inflammation of the thyroid gland due to a viral infection
107
what are the 4 phases of de quervains and how long does each last
1: hyperthyroidism 3-6 weeks
2: euthyroid 1-3 weeks
3: hypothyroidism weeks- months
4: euthyroidism
108
what is the presentation of de quervains thyroiditis (5)
painful goitre, neck pain, palpitations (common), difficulty eating and swallowing
109
what are the investigations for de quervains 2
1. thyroid function test- high free thyroxine index
2. high CRP in blood test
110
what are the two complications of de quervains
thyroid storm
long term hypothyroidism
111
what is the treatment for de quervains (2 parts)
hyperthyroid phase- NSAIDs and corticosteroids for pain and inflammation
hypothyroid phase- normally no treatment but if severe then levothyroxine can be given
112
differentials for de quervains (4)
graves
hashimotos
THYROID CANCER
TOXIC MULTINODULAR GOITRE
113
what are the main types of thyroid cancer and how many make up 98% of malignancies (4)- acronym
4 make up 98% of malignancies: papillary, follicular, anapaestic and medullary (people find art magnificent
114
risk factors of thyroid cancer (2)
head and neck irradiation and female sex
115
investigations for thyroid cancer (1st line, diagnosis)
1st line: ultrasound of neck
2. confirm with fine needle biopsy
116
2 treatment for thyroid cancer
1. thyroidectomy
2. radioactive iodine capsules to kill remaining cancer cells
117
complications of thyroidectomy (2)
increased risk of recurrent laryngeal nerve damage or hypoparathyroidism
118
what is thyroid storm an what is the alternative name for it
large amount of thyroid hormones released in a short amount of time
thyrotoxic crisis
119
symptoms of thyroid storm (4)
very high fever, profuse sweating, CV dysfunction, delerium
120
investigation and value for thyroid storm (1)
1. thyroid function test (low TSH, high serum thyroxine)
121
treatment for thyroid storm (2, GS)
1st: carbimazole
2nd: hydrocortisone (decreases T4->T3 conversion)
GS: thyroidectomy
122
what are the 3 pituitary adenomas
prolactinoma
acromegaly
cushings
123
what is cushings
increased cortisol levels
124
compare cushings disease and syndrome
cushings syndrome= set of symptoms due to cortisol excess in the body
cushings disease= cushings syndrome due to ATCH producing pituitary tumor
125
what are the two categories of causes of cushings
ACTH dependant and ACTH independant
126
what does ACTH stand for
adreno-corticotrophic hormone
127
causes of ACTH dependant cushings (2)
anterior pituitary adenoma and ectopic neoplasm (ussualy small cell lung cancer)
128
causes of ACTH independant cushings (2)
adrenal adenoma and oral steroids
129
symptoms of cushings (5)
round moon face
central obesity
red abdominal striae
proximal limb wasting
mood changes
(work from bottom of a person up in a straight line)
130
investigations for cushings (2, GS)
1st line: plasma cortisol- should be raised
2. 24 hour urinary free cortisol (more reliable)
GS: dexamethasone suppression test
131
investigations to diagnose individual CAUSES of cushings (3)
MRI- pituitary adenoma
chest CT- small cel lung cancer
abdominal CT- adrenal tumors
132
treatment for cushings 4
(hint all to do with causes)
1. stop steroids of steroid induced
2. adrenalectomy for adrenal adenoma
3. transsphenoidal surgery to remove pituitary adenoma
4. surgery if located ectopic neoplasm
133
4 complications of cushings
hypertension, CV disease, osteoporosis, diabetes mellitus
134
Explain the test results for dexamethasone suppresion and ACTH for:
-> adrenal adenoma
-> ectopic ACTH
-> cushings disease/ pituitary adenoma
-> adrenal adenoma
low dose test= low
high dose test= high
ACTH= low
-> ectopic ACTH
low dose test= low
high dose test= high
ACTH= high
-> cushings disease/ pituitary adenoma
low dose test= low
high dose test= low
135
what is aromegaly
high growth hormone secretion
136
causes of acromegaly (2)
benign anterior pituitary adenoma
ectopic secretion secondary to a lung/ pancreatic malignancy
137
how does excess GH cause inappropriate growth in aromegaly 2
excess GH causes inappropriate growth by directly acting on tissues and soft bones and indirectly by inducing insulin-like factor 1
138
symptoms of acromegaly (5)
BI TEMPORAL HAEMIANOPIA
large spade like hands and feet
ACROPARAESTHESIS- tingling/numbness in extremities
prominent forehead, jaw and chin
sleep apnea (enlarged tongue causes airway obstruction)
(work from top of a person down)
139
investigations for acromegaly and expected + results (1st, imagery, GS)
1st line: insulin-like growth factor 1 test (IGF-1)- should be high
GS: oral glucose TOLERANCE test
give patient glucose and normally serum GH should decrease
in individuals with acromegaly, GH levels do not decrease
2. brain MRI for imaging of pituitary tumors
140
treatment for acromegaly (4 lines, two alternatives for first depending on cause of acromegaly)
1st line: gold standard: trans-sphenoidal resection surgery of the pituitary tumour for acromegaly caused by pituitary adenomas
1st line: for acromegaly secondary to cancer, surgical removal of the cancer is the treatment
2nd line: somatostatin analogues: block GH release eg ocreotide
3rd line: GH antagonist to be given SC daily eg pegvisomant
4th line: dopamine agonists to block GH release eg bromocriptine
141
why is somatostatin, high levels of glucose and dopamine used in treatment of acromegaly
all inhibit growth hormone release
142
what are the complications of acromegaly (5)
T2DM- due to high levels glucose
heart disease- due to hypertrophy of heart caused by high GH levels
hypertension
ARTHRITIS- due to overgrowth of cartilage
bitemporal hemianopia- due to comppression of optic chiasm
143
what is excess secretion of GH before adolescence called 1
gigantism
144
where is prolactin made and by what
lactrotrophs in anterior pituitary
145
who typically has low 2 and high 2 prolactin levels
low= men and non-pregnancy women
high= pregnant women and new mothers
146
what does a prolactinoma produce
excess prolactin
147
causes of prolactinoma (2)
benign pituitary adenoma, antidoperminergic drugs
148
risk factors for prolactinoma (2)
biological female sex
peak incidence during childbearing years (20-40 years)
149
presentation of prolactinoma in both males and females (2)
low libido
galactorrhea
150
presentation of prolactinoma in males (3)
low testosterone
erectile dysfunction
reeduced facial hair
151
presentation of prolactinoma in females 2
a/oligomenorrhoea
increasde facial hair
152
why do high prolactin levels cause issues with hypogonadism
prolactin hypersecretion inhibits gonadotrophin-releasing hormones= inhibit FSH and LH, causing hypogonadism
153
investigations for prolactinoma (2)
1st: serum prolactin levels- high
2. pituitary MRI for adenoma detection
154
what is the most effective approach to prolactinoma treatment?
medicinal not surgical approach
155
treatment for prolactinoma (2)
1. dopamine agonists eg cabergoline
2. transphenoidal resection surgery of pituitary gland for adenoma
156
why are dopamine agonists effective in treating prolactinoma and what does it do to the prolactinoma
dopamine inhibits prolactin release and therefore this will cause shrinkage of the prolactinoma
157
what are the complications of prolactinoma (3)
infertility
sight loss/ raised intercranial pressure due to adenoma growth in the brain
158
what type of hormone is aldosterone
mineralcorticoid
159
what are the two main actions of aldosterone in the kidney and from where does this occur in the kidney
increases sodium reabsorption from distal tubule
increases potassium excretion from distal tubule
160
name the 5 layers of the adrenal gland (from out to in) and what hormones are produced by them and what type of hormone (4)
capsule
zona glomerulosa- mineralcorticoid, aldosterone
zona fasciculata- glucocorticoids eg cortisol
zona reticularis- androgens eg sex hormone
medulla- CATELCHOLAMINES eg adrenaline
161
what is conns and what is produced in excess in this condition 1
primary hyperaldosteronism with excess production of aldosterone
162
what organ is responsible for the abnormality in conns
adrenal glands are directly responsible for excess aldosterone production
163
2 causes of Conns- which is more common
bilateral adrenal hyperplasia (common) or adrenal adenoma
164
what is secondary hyperaldosteronism and what are the causes for this 2
excess renin levels cause the adrenal glands to produce more aldosterone
1. due to increased activation of RAAS system
2. due to renal artery stenosis
165
explain the pathophysiology of conns starting with the effect of high aldosterone (mention the negative feedback with renin)
aldosterone causes increased sodium reabsorption and therefore water reabsorption, causing high bp. Juxataglomerular cells detect this and releases less renin
166
symptoms of conns (5)
hypertension
headaches
hypokalaemia symptoms (due to renal excretions)- cramps, polyuria, nocturia
Mr conns owned 3 horses
167
what are the 3 investigations and results for conns (inc GS)
FBC, U&E should show low plasma protein and high aldosterone and low renin ratio, low K+
GS: selective ADRENAL venous sampling
168
what is the purpose of selective adrenal venous sampling
detects if there is bi/unilateral secretion from adrenal glands
169
what is the treatment for conns (1st, 2nd-2)
1. aldosterone antagonists eg spinonolactone
2.. treat cause eg adrenal adenoma= adrenalectomy or percutaenous renal artery angioplasty via femoral artery to treat renal artery stenosis
170
what is adrenal insufficiency and what organ secretes this
not enough cortisol and aldosterone produced by adrenal gland
171
what can adrenal insufficiency be classed as medically?
life-threatening
172
what are the three categories of adrenal insufficiency and which one is addisons
primary secondary and tertiary
addisons is primary
173
explain what happens secondary adrenal insufficiency and what does this lead to 2
inadequate ACTH stimulating the adrenal glands so less aldosterone and cortisol is released
174
explain what happens in tertiary adrenal insufficiency
inadequate CRH release by hypothalamus= less ACTH= less cortisol and aldosterone
175
causes of addisons (2) and where r the most prominent in the world
autoimmune adrenalitis (most common in developed)
TB (common in developing)
176
cause of secondary adrenal insufficiency 2
pituitary gland trauma or tumor
177
cause of tertiary adrenal insufficiency 1
long term oral steroids (more than 3 weeks) which suppresses the hypothalamus
178
what r the sodium and potassium electrolyte levels in addisons
hyponatremia and hyperkalaemia
179
non-specific symptoms of adrenal insufficiency (4)/ addisons (1)
non-specific: fatigue, hypotension, nausea and vomiting
Addisons- hyperpigmnetation in palmar creases
180
investigations and results for adrenal insufficiency (GS, 1st->4)
2 results for addisons specifically
GS- short synacthen
1st- FBC shows low cortisol, low aldosterone, low sodium and high potassium, (high renin and high ACTH for addisons specifically)
181
what is the treatment for adrenal insufficiency, what do they replace (2)
hydrocortisone to replace cortisol
fludrocortisone to replace aldosterone
182
what does fludrocortisone correct in adrenal insufficiency and how does it do this (in terms of electrolytes
will correct postural hypotension by increase Na+ and decreasing K+
183
explain the short synacthen test (2 steps and positive result)
1. give synthetic ACTH in the morning
2. measure cortisol levels at baseline, 30 and 60 minutes after admininistration
+ result: cortisol fails to rise to double the baseline
184
main complication of adrenal insufficiency (two alternative names)
adrenal/ Addisonian crisis
185
what is addisonian crisis
severe deficiency of adrenal steroid hormones eg cortisol and aldosterone
186
what are the consequences of an addisonian crisis (3)
can cause renal failure and hypvolemic shock
takes the HPA axis 6-12 months to recover
187
treatment for addisonian crisis 3 steps
1. immediate hydrcortisone injection
2. saline
3. bolus and top up of hydrocortisone via IV
188
what is SIADH and what does it stand for
syndrome of inappropriate ADH secretion
excessive ADH secretion
189
causes of SIADH (6)- acronym
post-operation, resp infection and meningitis, malignancy, trauma, meds (NSAIDs, thiazide, carbimazole)
MPs R Measly Tiny Mistakes
190
explain why patients with SIADH have low serum osmolarity but high urine osmolarity
1. excessive water reabsorption in collecting ducts
2.blood is diluted= hyponatraemia=low serum osmolarity.
3. less water is excreted is by kidneys= concentrated urine with high urine sodium levels= high urine osmolarity
191
what is euvolemic hyponatraemia and why does this occur in SIADH
there is still a normal amount of sodium in the body but hyponatraemia occurs because there is a large volume of water in the body, it dilute it
192
symptoms of SIADH (4)
heacheaches
fatigue
confusion
muscle cramps
3 to do with head and 1 with muscles
193
what are the consequences of severe hyponatraemia (2)
seizures and reduced consciousness
194
investigations for SIADH (2)
U&E (bloods)- hyponatraemia, low serum osmolarity
urine- high serum osmolarity
195
treatment management for SIADH 2
treatment for chronic SIADH 1
1. treat cause
2. fluid restriction to 500ml-1L
3. ADH receptor antagonist for chronic SIADH eg tolvaptan
196
complication of treating SIADH and how can this be avoided
central pontine MYELINOLYSIS
this can be avoided if sodium levels are corrected slowly
197
what are the two types of diabetes insipidus and which is most common
cranial and nephrogenic
cranial is most common
198
explain what happens in the the two types of diabetes insipidus
cranial diabetes insipidus: decreased secretion of ADH from posterior pituitary
nephrogenic diabetes insipidus: insensitivity to ADH in the collecting ducts of the kidney
199
causes of cranial DI (3)
brain tumors/ trauma/ infections
200
causes of nephrogenic DI (5)
INHERITED ADH RECEPTOR MUTATION, LITHIUM MEDICATION, chronic kidney disease, hypokalaemia and hypercalcaemia
CHHIL
201
explain why DI causes polyuria
ADH deficiency= less water reabsorbed= large volumes of dilute urine: polyuria
202
symptoms of DI (4)
polyuria, polydipsia, dehydration, hypotension
203
investigations for DI and results (GS with results, EXLCUSION)
GS- water deprivation test-low urine osmolarity and high serum osmolarity cranial
exclusion of DM with serum glucose test- normal
204
treatment for DI (2 general and 1 specific for each) include drug names where necessary
1. treat cause
2. rehydration with saline
cranial: desmopressin- syntehstic ADH
nephrogenic- thiazide diuretics eg oral bendroflumethiazide
205
what is hyperparathyroidism, from what cells where
excessive secretion of parathyroid hormone from chief cells in parathyroid
206
what are the three types of hyperparathyroidism and which is most common
primary secondary and tertiary
primary is most common
207
explain primary hyperparathyroidism and what can it cause 1
issue parathyroid glands which leads to additional secretive tissue, causing excess PTH production and therefore hypercalcaemia
208
what are the three causes of primary hyperparathyroidism and what percentage of cases do they contribute to
adenoma 80
hyperplasia of glands 20
parathyroid cancer 0.5
209
explain secondary hyperparathyroidism and how does the body compensate for this, what change happens to the parathyroid gland
insufficient vitamin D or CKD causes low absorption of calcium from the intestines, kidneys and bones= hypocalcaemia and makes the parathyroid gland release more PTH and undergoes hyperplasia to increase PTH secretion
210
what are the two causes of secondary hyperparathyroidism
chronic kidney disease and insufficient vit D
211
explain tertiary hyperparathyroidism
glands become autonomous, produce excessive PTH even after hypocalcaemia is corrected and doesn’t respond to negative feedback
212
when does tertiary hyperparathyoidism occur and what is the cause behind this reason
usually occurs after prolonged secondary hyperparathyroidism
common cause= kidney disease
213
what are the 3 effects of PTH and vitamin D on the body
PTH causes increased intestinal absorption of calcium, increased renal calcium reabsorption and increased absorption of calcium by osteoclasts in bones
214
risk factors for hyperparathyroidism (2)
elderly women (after menopause)
individuals with severe/ prolonged calcium or vitamin D deficiency
215
symptoms of hyperparathyroidism 4
same as hypercalcaemia- renal stones, painful bones, abdominal groans and psychiatric moans
216
what three things does abdominal groans encompass
constipation
nausea
vomiting
217
what three things does psychiatric moans encompass
fatigue
depression
psychosis
218
what is the investigation for hyperparathyroidism 1
PTH, calcium and phosphate profile test
219
what r the calcium, PTH and phosphate lab results for primary hyperparathyroidism
high calcium
high PTH
low phosphate
220
what r the calcium, PTH and phosphate lab results for secondary hyperparathyroidism
low/ normal calcium
high PTH
high/ normal phosphate
221
what r the calcium, PTH and phosphate lab results for tertiary hyperparathyroidism
high calcium
very high PTH
high phosphate
222
how are stones and bones investigated
detect stones: ultrasound for kidney stones
detect bones: DEXA scan for osteoporosis
223
what is a way of detecting adenomas
radioisotope scanning
224
what is the treatment for each type of hyperparathyroidism
primary: surgical removal of tumour
secondary: treat vitamin D deficiency or kidney transplant in individuals with CKD. A low phosphate diet is also recommended
tertiary: total or subtotal parathyroidectomy and/or calcimimetic: eg cinacalet
225
what do calcimimetics work
increase the sensitivity of parathyroid cells to Ca2+, causing less PTH secretion
226
what 2 values defines hypocalcaemia
<8.5mg/dL/<2.2mmol/L
227
what are the causes of hypocalcaemia (4)
thyroidectomy
chronic kidney disease
vitamin D deficiency
HYPERVENTILATION
228
what can cause hypocalcaemia that's not responsive to treatment and how can this be prevented
low magnesium levels
monitor magnesium levels
229
what is the pathophysiology of the hypocalcaemia in regards to neurones
low calcium levels increase neuronal excitability because it decreases the action potential threshold by reducing extracellular calcium
230
what are the symptoms of hypocalcaemia (10)- acronym
SPASMODICC
spasm
paraesthesia
anxious
seizures
muscle tone increased
orientation impaired (confusion)
dermatitis
impetigo herpetiformis
chvostek's sign
cardiomyopathy (long QT interval)
231
what are the 2 investigations and results for hypocalcaemia
blood test: low calcium, high PTH
ECG- shows prolonged QT interval
232
what is the treatment for severe hypocalcaemia (2)
IV calcium gluconate, 10ml of 10% solution over 10 minutes or IV calcium chloride
233
what is the treatment for persistent hypocalcaemia (1)
vitamin D supplement
50000 IU orally once a week for 8 weeks)
234
what are the two complications of hypocalcaemia
seizures and cardiac arrest
235
what are the two values that define hypercalcaemia
>10.5mg/dL or >2.6mmol/L
236
what are the causes of hypercalcaemia (4)
primary hyperparathyroidism
alcohol
excess vitamin D
sarcoidosis
237
what is the pathophysiology of the hypercalcaemia in regards to neurones
high extra cellular calcium inhibit sodium channels and reduce neural excitability
238
symptoms of hypercalcaemia (6) acronym
muscle weakness, decreased muscle tone, constipation, confusion, bone aches, lethargy
my mum counts calcium blood levels
239
investigations for hypercalcaemia (2)
fasting serum calcium and phosphate samples (high calcium, low phosphate)
24 hours urinary calcium
240
what happens to phosphate levels when calcium levels are high and low
high= low phospahte
low= high phosphate
241
treatment for hypercalcaemia (3)
1st line: rehydration with 0.9% NaCl
infused bisphosphonates in saline (these inhibits bone resorption) eg zolendronic acid 4mg
loop diuretics such as furosemide r sometimes used
242
what are the changes on an ECG for hypo and hypercalcaemia (1 each)
hypercalaemia= short QT
hypocalcaemia= long QT
243
what value defines hypokalaemia
<3.5mmol/L
244
what three main categories of causes cause hypokalaemia
decreased K+ intake
increased K+ excretion
K+ net movement extra-> intracellular
245
give examples of things that can cause decreased K+ intake (2)
K+ deficiency in diet
liqourice
246
give examples of things that can cause increased potassium entry into cells (3)
drugs eg insulin and B2 agonists (SABA/LABA)
metabolic alkalosis
247
give examples of things that can cause increased potassium excretion (4)
diuretics, vomiting, diarrhoea, Conn’s (hyperaldosteronism)
248
what can cause hypokalaemia with alkalosis (2)
vomiting and diuretics (fluid loss of acids)
249
what can cause hypokalaemia with acidosis (2)
partially treated DKA, diarrhoea
250
what is the pathophysiological effect of hypokalaemia regarding
1. neurones in the body and
2. neurones in the heart
in body, low K+ causes hyperpolorisation in cells which decreases neural excitability
in heart, it increases myocardial excitability, causing faster phase 4 depolorisation and tachycardia
251
symptoms of hypokalaemia (4)- saying to remember this
muscle weakness, palpitations, tetany (intermittent muscle spasms), tachycardia
Time for diMinished Potassium Time
252
what are the investigations for hypokalaemia 2 and how is it useful in identifying the cause of hypokalaemia (2)
FBC and U&E
latter can differentiate between renal and non-renal causes of hypokalaemia
253
what does hypokalaemia look like on an ECG (4)- saying to remember this
hypokalaemia: long PR interval, ST depression, flat T waves, prominent U waves
Time's Up Small Potassium
254
what is the treatment for mild/moderate hypokalaemia and what value is this
3.0-3.4mmol/L
oral replacement of K+
255
what is the treatment for more severe hypokalaemia (2) and what value is this
under 3mmol/L
IV replacement 40mmol KCL in 1L 0.9 NaCl salin solution
aldosterone antagonist if required (spironolactone)nd
256
what are the complications of hypokalaemia 4
MI, arryhthmia, muscle weakness and rhabomyolysis
257
what is the value that defines hyperkalaemia
>5.5mmol/L
258
what are the causes of hyperkalaemia (6)
excessive potassium intake
excessive endogenous potassium production
redistribution of potassium from intra to extracellular
decreased potassium excretion
Addison’s
ACE inhibitors
(4 to do with K+, 2 starting with A)
259
explain the pathophysiology of hyperkalaemia regarding neurones (acute hyperkaelamia and longer periods of hyperkalaemia)
acute: high K+ levels increase resting potential, making it easier to reach threshold for depolorisation= increased neural excitability
longer periods of hyperkalaemia: the body reduces the number of sodium channels, causing slower impulse conduction and decrease in excitability
260
symptoms of hyperkalaemia (4)- saying to remember this
fast irregular pulse, chest pain, muscle weakness and paralysis
crikey! problems of more potassium
261
investigations for hyperkalaemia (3)
ECG
high serum potassium
urine electrolytes: high urine potassium
262
what are the ECG changes seen in hyperkalaemia (3)
hyperkalaemia: tall tented T waves, small/ skipped P waves, wide QRS complex, prolonged PR interval
263
management plan for treating hyperkalaemia 3
1. treat cause
2. if cardiotoxic changes on ECG give IV calcium gluconate/ chloride
3. if no cardiotoxic changes on ECG, given combined insulin/ dextrose infusion with nebulised salbutamol
264
how can potassium be medically removed from the body (3)
calcium resonium, loop diuretics or dialysis
265
why do cardiotoxic changes matter so much in treating hyperkalaemia
cardiotoxic- IV calcium given which doesn't reduce serum K+ levels to prevent heart complications and stabilise the myocardium
not cardiotoxic- shifts K+ from extra to intracellular
266
when is emergency treatment required for hyperkalaemia
severe hyperkalaemia (>6.5mmol/L)
267
what are the complications of hyperkalaemia 1
if untreated it can cause life-threatening arrythmias
268
name the two endocrine tumors
carcinoid tumor
Phaeochromocytoma
269
what is carcinoid tumor and what cells release this
malignant enterochromaffin cells release 5-hydroxytryptamine (serotonin) in systemic circulation
270
what is the common origins of carcinoid tumor and what part is the most common for origin
commonly from GI tract
most common= small intestine malignancy (ileum)
271
explain why some people get symptoms and some do not for carcinoid
the excess serotonin secreted enters the enterohepatic circulation and the liver inactivated the hormones, causing no symptoms
however, when liver metastasis are present, hormone secretion into the circulation causes symptoms due to liver dysfunction
272
symptoms of carcinoid tumors (6)
diarrhoea, stomach pain, loss of appetite, weight loss, palpitations, flushing
DAS War PerFect
273
investigations for carcinoid tumor (2)
1st line: urinary 5-hydroxyindoleactic acid level- high
Imagery: chest x-ray and chest/pelvic MRI to locate primary tumors
hydroxyindoleactic= (hydroxy, a girl named leah from indonesia with ticks
274
GS diagnostic test for carcinoid tumor and what is the positive result
chromogranin A (should be elevated in serum)
275
treatment and how do they work for carcinoid tumor (3)
1. surgery: resection of a tumour is the only cure for carcinoid tumors= vital to find 1’ tumour
2. somatostatin analogues: octreotide: reduces serotonin release, therefore, reduces symptoms
3. radiotherapy for hepatic masse can decrease symptoms
276
what is Phaeochromocytoma
excess production of adrenaline and noradrenaline
277
what can Phaeochromocytoma be classed as medically?
life threatening
278
cause of Phaeochromocytoma (1) (include what cell and what origin this has)
benign neoplasm of adrenal gland’s chromaffinin cells (medullary origin)
279
symptoms of Phaeochromocytoma (4)
tacchycardia, hypertension, sudden attack that increase in duration, tremor
Sameera, try the hype
280
what is the 1st line/ diagnostic investigation for phaeochromocytoma 1
plasma metanephrines
281
treatment for Phaeochromocytoma (1)
laparoscopic surgery/ open surgery for tumour removal
282
what are the 3 main ways that skin conditions can be diagnosed/ investigated
clinical observation, swabs or biopsy
283
what does the water deprivation test show for cranial diabetes insipidus and why
low urine osmolarity after fluid deprivation but high after desmopressin (responds to synthetic ADH which is desmopressin= concentrated urine)
284
what does the water deprivation test show for nephrogenic diabetes insipidus and why
low urine osmolarity after fluid deprivation and desmopressin (as kidneys insensitive to ADH)
285
How to do the short synacthen test 3 and what are the ACTH baseline values for primary and secondary adrenal insufficieny
1. measure basal cortisol at 9am
2. administer synacthen (synthetic ACTH)
3. sample cortisol after 30 mins
primary= high ACTH
secondary= low ACTH
286
what is a marker of addisons disease
21-hydroxylase antibodies
287
what condition has hyperpigmentation
addisons
288
what is the most common site for carcinoid tumuors to metastasise 1
liver
289
side effects of metformin 3
lactic acidosis, liver failure, abdominal pain
290
side effects of SGLT 2 inhibitor 3
DKA, UTI, back pain
291
piaglitazone side effects 2
bladder cancer, bone fractures
292
what is a key acromegaly complication 1 and how does this present 3
carpal tunnel syndrome
numbness/ tingling/ pain across median nerve supplied dermatome
293
what r the 3 test values for DKA
ketones >3mmol, pH <7.3, glucose >11
294
how do u chose between IV glucose and glycogen as a hypoglycaemia treatment and give an example
based on their stores
eg a man who’s been really ill for long period of time in hospital= doesn’t have much glucose store then give him glucose IV
295
what is the first line treatment for phaechromocytoma hypertensive crises and how does this work
phentolamine- blocks alpha adrenergic receptors leading to vasodilation
296
what is the leading cause of hypothyroidism in the developed and developing world
developed- hashimotos
developing- iodine deficiency
297
what r the categories and subcategories of diabetes mellitus complicaitons
acute= DKA and HHS
chronic= microvascualr and macrovascular and diabetic ulcers
298
what is a consequence of untreated hyperkalaemia 1 and explain why
ventricular tachycardia (cell membranes become partially depolarised= the ventricles contract faster)
299
what r the TFT values for graves/ thyrotoxicosis
low TSH, high T4
300
what r the TFT values for subclinical hypothyroidism and hyperthyroidism
hypo= high TSH and normal T4
hyper= low TSH and normal T4
301
what r the TFT values for hashimotos/ primary hypothyroidism
high TSH, low T4
302
what r the TFT values for secondary hypothyroidism (pituitary mass causing hypothyroidism) and explain the pathophysiology
low TSH, low T4
pituitary mass compresses TSH secreting cells causing low TSH levels
303
what combination of three things can lead to hypocalcaemia (2 endogenous, 1 exogenous)
chemotherapy
renal cell carcinoma
lack of vit D
304
what axis does cushings interrupt
HPA
305
what is used as a screening marker for thyroid cancer reoccurrance
serum calcitonin
306
what r the symptoms of primary hyperparathyroidism 3
colicky abdominal pain, constipation, depressed mood
307
compare calcium levels for primary secondary and tertiary hyperparathyroidism
high calcium= primary hyperpara
low calcium= secondary hyperpara
high calcium= tertiary hyperpara
308
what three things indicate SIADH
small cell lung cancer
and
high plasma sodium
confusion, nausea and vomiting (symptoms that point towards high sodium)
