Week one Flashcards

Haem, cardiovascular, endocrine (136 cards)

1
Q

Where are corticosteroids made in the adrenal?

A

cortex

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2
Q

Where are the catecholamines made in the adrenal?

A

medulla

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3
Q

What is CRH and where is it released?

A

corticotropin releasing hormone
from the hypothalamus

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4
Q

Where is ACTH released from and what is it’s full name?

A

anterior pituitary gland and adrenocorticotropic hormone

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5
Q

What does ACTH stimulate release of?

A

cortisol

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6
Q

Why are ACTH and CRH increased in pregnancy?

A

produced by the placenta as well
increase in cortisol binding globulin stimulated by estrogen

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7
Q

Why don’t fetuses get adrenal suppression from maternal steroids?

A

the placenta inactivates them
11b hydroxysteroid dehydrogenase ? CTP says it does in cushings

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8
Q

What hormones are released from the APG?

A

GH, PRL, TSH, ACTH, FSH, LH

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9
Q

What is released in the PPG?

A

ADH, oxytocin

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10
Q

How much does prolactin in crease in pregnancy and when?

A

from early T1, 10 fold eventually

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11
Q

What hormone is similar in structure to GH?

A

human placental lactogen

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12
Q

What happens to levels of ADH in pregnancy?

A

stay the same

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13
Q

How much for serum and urinary free cortisol increase by term?

A

3 fold

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14
Q

What is a glucocorticoid?

A

(controls metabolism, immune response) cortisol

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15
Q

What is a mineralocorticoid?

A

(controls salt, water, BP) aldosterone

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16
Q

Where is renin releases from?

A

kidneys

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17
Q

What does renin do?

A

converts angiotensinogen to angiotensin I

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18
Q

What does angiotensin converting enzyme do?

A

converts angiotensin I to II in the lungs

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19
Q

What does angiotensin II do?

A

causes vaso constriction, heart remodelling and aldosterone release from the adrenal glands

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20
Q

What does aldosterone do?

A

increases na reabsorbtion, K secretion and H+ secretion
causing increase in fluid retention

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21
Q

What happens to levels of aldosterone in pregnancy?

A

increased 10 fold by term

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22
Q

What is conns syndrome?

A

primary hyperaldosteronism due to an adrenal adenoma, hyperplasia or malignancy

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23
Q

What signs do you see with conns syndrome?

A

HTN, low K, metabolic alkalosis

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24
Q

How do you diagnose conns syndrome?

A

difficult to interpret aldosterone: renin so order MRI or USS

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25
how does spironolactone work?
aldosterone antagonists, do not give in pregnancy as causes under virilisation of male fetus
26
Where is ADH made?
HT
27
What stimulates ADH to be made?
high sodium levels or low blood volume
28
what does ADH do?
works on distal collecting tubule to resorb water and also causes some vasoconstriction, acts to reduce osmolarity
29
what is the difference between how ADH and aldosterone increase fluid?
aldosterone brings Na in and K out.
30
What can happen to prolactinomas in pregnancy and what adverse outcomes occur with the pregnancy?
they can grow, but no adverse out come on pregnancy
31
Can you breast feed with prolactinoma?
yes but if enlarging may need to stop to go onto carbergoline or bromocriptine
32
What is the primary inhibitor of prolactin?
dopamine
33
What can cause raised prolactin?
* Normal pregnancy * prolactinoma * Hypothalamic or pituitary stalk lesions (removal on dopaminergic suppression of prolactin) * Empty sella syndrome * Hypothyroidism (TSH stimulates lactotrophs) * CKD * Seizures Drugs - metoclopramide
34
How would you diagnose prolactinoma in pregnancy?
MRI or CT
35
What proportion of women with prolactinomas will experience remission after pregnancy and breastfeeding?
>40%, more common for micro
36
What are the four kinds of diabetes insipdus?
1. central 2. nephrogenic 3. transient 4. psychogenic
37
What is central diabetes insipidus? causes?
lack of ADH production - prolactinoma pressure, sheehans syndrome, trauma, TB
38
What is nephrogenic DI? Causes?
insensitivity to ADH in kidneys. caused by CKD, lithium, hypercalcemia
39
What is transient DI? cause?
due to increased vasopressinase by placenta or reduced breakdown of vasopressinase in liver. from HELLP AFLD,
40
How do you treat DI central?
DDAVP, desmopressin acetate. ADH artificial
41
How do you treat DI nephrogenic?
water intake up to 20L per day
42
How can you tell if someone has DI?
unable to appropriately concentrate urine with water deprivation, unable to do in pregnancy easily
43
What can happen in severe cases of DI?
seizures and oligohydrmanios
44
What complications in pregnancy are seen with acromegaly?
HTN and DM, macrosomia
45
How do you treat acromegaly?
dopamine receptor agonists (ework 50%), octreotide (limited safety profile in pregnancy), transphenoidal resection
46
What are the causes of hypopituiatrism?
sheehans syndrome, pituitary adenoma, lymphocytic hypophysitis, radiotherapy
47
What symptoms do you get with hypopituitarism?
failure of lactation, persistent amenorrhoea, loss of pubic hair, hypothyroidism, aderenocorticoid insufficiency
48
What hormones do you replace in hypopituitarism?
steroids with stress dosing, thyroxine, ADH, GH should be stopped in pregnancy
49
What part of the PG is most vulnerable to sheehans syndrome?
APG due to its significant hypertrophy in pregnancy
50
What is lymphocytic hypophysitis?
* AI condition with chronic inflammation of APG. Get oedema and fibrosis. Most common in late pregnancy and post partum. causes mass and hypopituitarism effects
51
Why do you not need aldosterone replaced in sheehans syndrome?
not APG dependent
52
What is the most common cause of cushings in pregnancy?
adrenal adenoma or carcinoma
53
at are the adverse outcomes in pregnancy related to cushings syndrome?
fetal loss, PTB, PN mortality, PET, fetal adrenal insufficiency, poor tissue healing
54
What is the treatment for cushings?
surgery, needs to happen in pregnancy to improve pregnancy outcomes
55
What is cushings disease?
increased cortisol from a pituitary adenoma releasing ACTH
56
What is conns syndrome? and what do you see on bloods
hyperaldosteronism - HTN and hypokalemia <3.0 and alkalosis
57
What can be the cause of primary hyperaldosteronism?
adrenal carcinoma adrenal aldosterone secreting adenoma bilateral adrenal hyperplasia
58
How do you diagnose conns syndrome in pregnancy?
imaging - MRI or USS hypokalemia supressed renin , high aldosterone (hard to interpret in pregnancy)
59
How do you manage conns syndrome?
K sparing diuretics, BP control if malignancy suspected surgery, otherwise defer until after pregnancy
60
What are the features of a phaeo?
paroxysms of palpitations, sweating, anxiety, pallor, chest pain, vomiting, glucose intolerance, headache, labile hypertension
61
what is the risk of pregnancy on phaeo?
fetal hypertensive crisis in labour, opiates, GA supine pressure on tumour may worsen hypertension
62
What is the risk of the phaeo to the pregnancy?
maternal death - pulmonary edema, CVD, arrhythmia. 15% death in labour is undiagnosed fetus - FGR, IUFD 30%, miscarriage, hypoxia abruption
63
What causes the fetal effects in phaeo?
the hormones do not significantly reach fetus due to placental cells containing hormones which brak these down. vasoconstriction of uterine artery, uteroplacental insufficiency
64
How do you diagnose a phaeo?
elevated 24-hr catecholamine and metabolites collection urine or serum + localisation of the tumour with USS/MRI adrenals
65
What is the maternal mortality rate in phaeo if undiagnosed or diagnosed?
17% vs 4%
66
What is the fetal mortality rate in phaeo if undiagnosed vs diagnosed?
26% vs 11%
67
How do you manage phaemochromocytoma?
1. first control BP with alpha blocker eg doxasocin 2. second control HR with beta blocker eg labetalol 3. surgery should be performed ideally <24 weeks or at time of delivery with alpha blockade prior 3/7 4. delivery by CS due to risk of malignant HTN
68
What is addisons disease?
Adrenocortical failure - causes mineralocorticoid and glucocorticoid deficiency
69
What are the symptoms of addisons?
weight loss, vomiting, lethargy, postural hypotension, hyperpigmentation
70
What blood results do you get with addisions?
high K, low Na, low glucose, high urea
71
How do you diagnose addisons?
low 0900 cortisol levels, high ACTH and blunted reponse to synacthen test remember to use pregnancy specific ranges
72
How do you manage addisons disease in pregnancy and labour?
Fludrocortisone (mineralocorticoid) and hydrocortisone maintenance Requires stress dosing and IVF PRN May get profound hypotension with diuresis post partum
73
What is congenital adrenal hyperplasia?
an inherited (recessive) group of disorders characterised by a deficiency of any of the enzymes needed for cortisol biosynthesis This results in: 1. deficiency in both aldosterone and cortisol 2. increased levels of cortisol precursors and androgens
74
What is the most common deficiency causing CAH?
21-hydroxylase 90%
75
What is the gene frequency and prevalence for CAH?
1 in 200-400 1 in 14 000 have it
76
What are the clinical features of classic CAH?
adrenal insufficiency in infancy masculisation of the female fetus salt losing crises of the male neonate (MC def) precocious puberty in the male
77
What are the features of non classic or late onset CAH?
PCOS, infertility, anovulation, hirsuite, acne, delayed menarche, premature menopause, can cause HTN is specific definiciencies, genital abnormalities
78
What are the risks to the pregnancy in CAH?
miscarriage, PET, CS for CPD, FGR, GDM
79
How do you maximise fertility in women with CAH?
suppression of hyperandrogegism with gluticocorticoids.
80
How do you manage CAH in pregnancy with an uneffected fetus?
The aim is to cause adrenal suppression 1. continue GC and MC treatment. prednisone is the GC of choice as it doesn't cross the placenta 2. monitor electrolytes and serum testosterone levels - if high should increase steroids 3. GC need increasing with stress and delivery 4. free floating testosterone should be metabolised to oestrogen by the placental aromatase
81
How do you manage CAH with a possibly effected fetus?
1. Treat with dexamethasone as this crosses the placenta to suppress fetal ACTH and avoid fetal female virilisation. start before 5 weeks 2. continue until sex of fetus is known, if female until end of pregnancy prevention of virilisation is not always successful
82
How do you manage a female fetus treated for CAH in utero?
need cortiosteroids as they will ne adrenal supressed from aternal dex and also to treat their CAH if present
83
What is the risk for a male fetus with CAH?
salt losing crises at birth
84
What happens to calcium levels in pregnancy?
free calcium stay the same, total Ca falls due to low albumin, increased urinary excretion and placental transfer to fetus
85
What happens to ca demands in pregnancy and lactation?
increase
86
how does your body make up for the increased Ca needs in pregnancy?
vitamin D mediated absorption from the gut increased
87
What is the active form of vitamin D and what do you need to make this from cholecalciferol?
calcitriol, liver and kidneys needed
88
What is the treatment for hyperparathyroidism in pregnancy?
fluid, phosphate supplements, low calcium
89
If hyperparathyroidsm is untreated what effect can occur for the fetus and neonate?
IUGR, IUFD, PTB and neonatal hypocalcaemia through fetal PTH suppression causing seizures or tetany due to suppression of fetal PTH with high Ca from mum
90
If hyperparathyroidsm is untreated what effect can occur for the the mother?
miscarriage, PET, pancreatitis, hypercalcemic crisis
91
What causes secondary hyperparathyroidism?
low Ca and vitamin D means you make more PTH to compensate and maintain calcium homeostasis
92
How do you treat hypoparathryodism?
1,25-hydroxylated vitamin D and calcium. requirements increase 2-3 fold in pregnancy
93
What are the fetal risks of hypoparathryroidism?
late miscarriage, fetal rickets, seizures
94
What are risk factors for vitamin D deficiency?
pigmented skin * Covered * Vegans * Short IPI * Obesity * Malabsorption * AEDs * Renal or liver disease ETOH abuse
95
What clinical features do you get with vit D deficiency?
* Bone loss * Low weight gain * Hypocalcemia * Osteomalacia/rickets * Myopathy * GDM PET/FGR/HTN
96
What are the treatment options for thrombophlebitis?
* Elevate leg * NSAID gel or oral * Analgesia * Conpression stocking * Warm compresses * Antibiotics if concern for infection * Clexane may be used to reduce clot and pain * puncture and evacuation
97
What are the common changes you get with oral disease in pregnancy?
1. Gingivitis - reversible, inflammation of the gums 2. Periodontitis - inflammation of the supporting structures of the tooth tissue around the teeth causing shrinkage of the gums and loosening of teeth, irreversible 3. Increase in caries due to increased streptococcus mutans in saliva. 4. Pyogenic granuloma - pregnancy tumour in the gingiva, vascular lesion from progesterone levels, T2 and T3 and rapidly regress post partum. 5. Dental erosion - from vomiting, get demineralisation of teeth and enamel erosion
98
What is periodonitis related to for pregnancy outcomes?
PTB and low birth weight. 2-3 x more likely. this doesn't change when treated ? causation or correlation with other health practices
99
What is the highest risk thrombophilia for VTE?
antithrombin deficiency
100
How is anti thrombin def with a history of VTE managed differently to other thrombophilias?
if previous VTE with ATD offered higher doses of clexane 50 to 75% of treatment dose. sometimes need antithrombin in pre delivery
101
If a women has recurrent VTE and no on anticoagulation, when in pregnancy should she start clexane?
as soon as possible
102
When should women with previous VTE have clexane from and to?
throughout the antenatal period to 6 weeks or when go back on their regular anticoagulant
103
Which women with previous VTE can consider having the clexane VTE Px withheld until 28 weeks?
if provoked by major surgery and fully recovered with no additional risk factors
104
If women who are asymptomatic with symptomatic antithrombin deficiency, Protein C or S deficiency or more than one thrombophilic defect (homozygous FVL, prothrombin gene mutation, compound heterozygote), what should you do for VTE Px?
refer to specialist to consider antenatal clexane, should have 6 weeks PN
105
What is the importance of asympyomatic antiphospholipid antibodies?
they are considered a risk factor taken into account with scoring
106
When is anti Xa monitoring needed?
is some treatment cases
107
is warfarin safe in BF?
yes
108
when can you change from clexane to warfarin PP?
when the bleeding risk if low, usually 5-7 days
109
When can you remove an epidural after clexane dose?
12 hour after
110
When can you give clexane after regional anaesthetics eg epidural removed or spinal complete?
4 hours
111
When can you give regional anaesthesia after prophylactic clexane dose?
12 hours
112
When can you give regional anaesthesia after treatment clexane dose?
24 hours
113
Why is LWMH preferred over UFH?
as lower risk of heparin induced thrombocytopenia equally effectiv
114
What is the reccomended prophylactic dose for AN and PN prphylaxis for women 91-130kg?
60mg daily
115
What is the reccomended prophylactic dose for AN and PN prphylaxis for women <50kg?
20mg
116
What are the benefits of UFH over LMWH?
shorter half life and reliable reversal agent (protamine sulphate) time between dose and regional anesthetics only 4 hours less risk of epidural haemtoma
117
What birth defects are linked with warfarin?
hypoplasia of nasal bridge, congenital heart defects, ventriculomegaly, agenesis of the corpus callosum, stippled epiphyses
118
what is the highest risk time for warfarin embryopathy and what is the % risk?
5% and 6-12 weeks
119
All emegrency CS should be considered for how long LMWH?
10 days
120
What is a high risk thrombophilia?
antithrombin deficiency, protein C or S deficiency, compound or homozygous for low risk thrombophilia
121
What is a low risk thrombophlia?
factor V Leiden heterozygote or prothrombin mutation heterozygote
122
What are the antenatal risk factors for scoring for VTE prophylaxis?
BMI >30 age >35 parity >2 smoker varicose veins PET immobilty FHx of unprovoked or estrogen provoed VTE low risk thrombophlis multiple pregnancy IVF/ART
123
How many antenatal risk factors do you need for prophylaxis from T1 and from 28 wekes?
4+ = T1 3 = from 28 weeks
124
What antenatal risk factors would make you intermediate risk to consider AN clexane?
hospital admission single previous VTE related to surgeyr high risk thrombophilia and no VTE hx medical comorbidities any surgical procedure OHSS T1 only
125
What are contraindications to celxane?
* Bleeding disorder * Active bleeding * At risk of major haemorrhage * Platelets <75 * Acute stroke in last 4 weeks * Severe renal (creat <30) or liver disease * Uncontrolled HTN SBP>200 or DBP >120
126
What do you treat MRSA colonisation with?
nasal ointment - mupirocin or fusidic acid 3-5 days antibacterial soaps
127
What do you treat active infection of MRSA with?
IV vancomycin oral clindamycin alternately daptomycin
128
What is chiari malformation?
A group of structural conditions characterised by congenital caudal displacement of the cerebellar tonsils below the foramen magnum, often associated with caudal displacement of the brainstem. syrinx, hydrocephalus
129
What is the pathogenesis of DIC?
1. procoagulant substances released due to endothelial injury - thromboplastin, phospholipid 2. consumption of clotting factors and platelets 3. massive fibrinolysis and FDPs prevent stable fibrin clot formation
130
How do you diagnose DIC from bloods?
low platelets low fibrinogen <2 high FDPs high soluble fibrin complexes abnormal coagulation profiles
131
How do you manage DIC?
treat underlying cause usually needs delivery treat coagulopathy
132
What does cryoprecipitate contain?
factor I (fibrinogen), factor VII, factor XIII, vWF, fibronectin
133
When does DIC usually resolve?
24-48 hours platelets can take up to a week
134
What are the diseases screened for on the guthrie card?
metabolic - phenylketonuria and maple syrup urine disease, MCAD, galactosaemia, biotinidase deficiency other - CAH, CF, congenital hypothyroidism, severe combined immunodeficiency, spinal muscular atrophy
135
When should guthrie card testing be done
24-48 hours of age, ideally before 72 hours
136
When should newborn hearing screening be done?
ideally less than one month but up to 3 months