Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Semester 1 ( 3rd Year) > Case 12: Abdominal distention and weight gain > Flashcards

Case 12: Abdominal distention and weight gain Flashcards

1
Q

what does ACTH stand for

A

adrenocorticotropic hormone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What does PRL stand for?

A

Prolactin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what does ADH stand for

A

antidiuretic hormone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

hormones produced by the posterior pituitary

A

oxytocin
ADH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

hormones produced by the anterior pituitary

A

TSH
GH
ACTH
FSH/LH
PRL
endorphines

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what is the target organ of oxytocin

A

uterine muscles of mammary glands

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what is the target organ of ADH

A

kidney tubules

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what is the target organ of TSH

A

thyroid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

what is the target organ of GH

A

entire body

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

what is the target organ of ACTH

A

adrenal cortex

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

what is the target organ of FSH/LH

A

testes and ovaries

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

what is the target organ of prolactin

A

mammary glands

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what is the target organ of endorphins

A

pain receptors in the brain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what structure which is immediately anterior to the pituitary gland produces the characteristic symptoms in those who have a large pituitary tumour

A

the optic chasm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

why does the optic chiasm show that there is a large pituitary tumour

A

it is compressed with large pituitary tumours
this is associated with bitemporal hemianopia (associated with enlarging pituitary lesion)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

what is the other name for the adrenal glands

A

suprarenal glands

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

what artery supplies the adrenal glands

A

suprarenal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

what are the 3 suprarenal arteries and where do they arise from

A

superior- inferior phrenic
middle- AA
inferior- renal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

what vein drains the suprarenal glands

A

left and right suprarenal veins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

where does the left suprarenal vein drain into?

A

left renal vein

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

where does the right suprarenal vein drain into

A

IVC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

3 most commonest causes of end stage renal disease in western countries

A

diabetes
hypertension
glomerular disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

the glomerulus structure from blood side to urine side consists of

A

endothelial cells
glomerular basement membrane
epithelial cells (podocytes)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

what is the glomerulus

A

tightly packed loop of capillaries

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

what supplies the glomerulus

A

afferent arteriole

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

what drains the glomerulus

A

efferent arterioles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

the bowmanns capsule is an extension of what

A

the Proximal tubule

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

what surrounds the glomerulus

A

bowmanns capsule

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

what cells play a role in regulating eGFR

A

mesangial cells (in the centre of the glomerulus)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

role of the mesangial cells

A

have contractile properties similar to vascular smooth muscle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

what type of kidney disease is polycystic kidney disease

A

autosomal dominat

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

what genes are effected in the polycystic kidney disease

A

autosomal dominant

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

what genes are affected in polycystic kidney disease

A

PDK1 (mostly)
PDK2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

what happens in polycystic kidney disease

A

small cysts lined by tubular epithelium develop from infancy or childhood and develop and enlarge slowly or irregularly

the surrounding normal kidney tissue is compressed and gradually damaged

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

is the PDK1 or PDK2 mutation worse

A

end stage kidney disease occurs in 50% of those with PDK1 and has an average onset of 52 years

minority of those with PDK2 get end stage kidney disease and average onset is 69 years

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

what % of patients on renal replacement therapy have polycystic kidney disease

A

5-10%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

what can be the result of podocyte injury

A

focal segmental glomerulosclerosis (FSGS)
minimal change disease
membranous nephropathy
(all categorised as nephrotic syndrome)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

pathogenesis of FSGS and minimal change disease

A

remains unknown
circulating factors may increase glomerular permeability and cause injury to podocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

pathogenesis of membranous nephropathy

A

antibodies attack podocyte surface antigen (phospholipase A2 receptor 1) with complement dependant podocyte injury

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

what type of syndrome is IgA nephropathy categorised as

A

nephritic syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

what cells are mainly targeted with IgA nephropathy rather than podocytes

A

mesangial cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

what decreases when albumin is lost in the urine?

A

plasma oncotic pressure (causes swelling)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

what would you want to know about a patients abdominal distension

A

how long

is it intermittent or constant

is it related to eating

is it lessened by belching or passing gas

associated with vomiting, loss of appetite, weight loss/gain, change in bowels, SOB, leg swelling

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

what should you ask about for CCF

A

how many pillows do they sleep on

do you get breathless if you slip off pillows- orthopnea

any history of cardiac issues/angina

do they wake up gasping for air at night

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

what should you ask about for chronic liver disease

A

how much alcohol

any skin bruising

any skin discolouration

any skin itching

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

what should you ask about for nephrotic syndrome

A

any ankle/leg swelling

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

what should you ask about for hypothyroidism

A

skin dryness

hair loss

sensitivity to cold

tiredness

constipation

low mood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

what should you ask about for metabolic syndrome

A

excessive thirst

passing lots of urine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

what should you ask about for cushings syndrome

A

any skin bruising

changes at the back of the neck

redness in the face

markings on the skin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

what is cushings syndrome

A

chronic glucorticoid (cortisol) excess, with loss of circadian rhythm of release

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

signs and symptoms of cushings syndrome

A

BG SOFAS

B- increased BP
G- increased glucose

S- skin bruising, purple abdominal striae (stretch marks), acne, hyperpigmentation (due to increased ACTH), poor wound healing

O- osteoporosis, achilles tendon rupture, proximal myopathy
F- fat face (moon face), central obesity, buffalo hump, wasted legs

A- affect, altered mood, lethargy, psychosis

S-sex, irregular menstruation, hirsutism (excess hair around mouth and chin), erectile dysfunction, gynaecomastia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

how to diagnose cushings syndrome

A

dexamethasone suppression test
24hr urine cortisol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

causes of cushings

A

iatrogenic (excess steroid use)

basophilic pituitary adenoma (cushings disease)- usually onset of 25-50

ectopic ACTH syndrome- small cell lung cancer, pancreatic or thyme carcinoid tumour

adrenal adenoma

adrenal adenocarcinoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

what is the criteria for metabolic syndrome

A

high glucose

abdomail obesity

high BP

low levels of HDL cholesterol

hypertriglyceridaemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

what is normal BMI

A

18.5-24.9

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

what is overweight BMI

A

25-29.9

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

what is obesity I BMI

A

30-34.9

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

what is obesity II BMI

A

35-39.9

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

what is obesity III BMI

A

40+

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

what BMI is considered a risk for black African and Carribean and Asian people

A

23 is increased risk
27.5 is high risk

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

what is orlistat

A

pancreatic lipase inhibitor

used for obesity

reduces fat absorption

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

what is liraglutide (saxenda)

A

GLP-1 analogue (agonist)

used for weight management and T2D

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

when would you offer surgery for obesity

A

if BMI over 40

or

if BMI 35-40 with other significant weight related disease

if all non-surgical options have been attempted

has been or is willing to receive tier 3 weight management services

fit for anaesthesia and surgery

person commits to need for long-term follow-up

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

how does the dexamethasone suppression test work

A

dexamethasone is an exogenous steroid which supresses the pituitary through negative feedback

it binds to glucorticoid receptors in the pituitary inhibiting ACTH release by the pituitary

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

what are the results of the dexamethasone test normally and what is pathological

A

normal= reduction in cortisol with low-dose

cushings= no reduction in cortisol output with low dose, but reduction with high-dose

adrenal tumour or ectopic ACTH= no reduction in steroid production after low or high dose

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

what is cyclical cushings

A

very rare

characterised by alternating excess or normal endogenous cortisol secretion

has variable clinical features

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

what do to if you suspect cyclical cushings

A

repeat follow up testing is required

urinary cortisol or late-night salivary cortisol are preferred for screening

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

when do you do dexamethasone test

A

overnight

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

what are the 2 classifications of cushings syndrome

A

ACTH dependent
ACTH independent

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

is ACTH dependant or independent more common

A

dependent

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

ACTH dependant causes of cushings syndrome

A

pituitary adenoma (cushings disease)= 65-70%

ectopic ACTH= 5-10% (bronchial carcinoid is most common)

unknown source of ACTH= less than 1%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

ACTH independant causes of cushings syndrome

A

adrenal adenoma= 10=18%

adrenal carcinoma= 6-8%

adrenal hyperplasia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

what would you do next if you thought someone has cushings and has a raised cortisol despite dexamethasone suppression test

A

measure ACTH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

what are the consequences of removing the anterior pituitary and how can we solve this

A

hormones produced by the anterior pituitary need to be replaced:

TSH- give thyroxine
GH- some might get GH therapy
ACTH- hydrocortisone therapy
FSH/LH- testosterone or oestrogen/progesterone therapy

some might need desmopressin (synthetic ADH) where ADH secretion is affected because of damage to the posterior pituitary or hypothalamus causing diabetes insipidus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

what hormones do not need to be replaced when removing the anterior pituitary

A

prolactin

ADH, endorphins, oxytocin don’t need to be replaced as they are stored by the pituitary not produced

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

what size is considered a pituitary microadenoma

A

<1cm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

what size is considered pituitary macroadenoma?

A

> 1cm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

when would you call it cushings disease

A

when it results from a pituitary adenoma causing excess ACTH release

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

what gland releases cortisol

A

adrenal gland

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

what is the negative feedback loop for cortisol production

A

the hypothalamus releases CRH

this acts on the pituitary to release ACTH (ACTH has -ve feedback on hypothalamus)

this acts on the adrenal gland to produce cortisol (cortisol has -ve feedback on the pituitary)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

in which area of the adrenal cortex is cortisol produced

A

zona fasiculata

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

when do cortisol levels peak

A

in the morning (when we need to get up)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

when do cortisol levels drop

A

at night (when we need to sleep)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

what processes to cortisol stimulate

A

gluconeogenesis
lipolysis
proteolysis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

what affects does increased cortisol have on the body

A

vasoconstriction (increases sensitivity to A and NA)

decreased immune response (low T-lymphocytes and prostaglandins)

decreases mood and memory

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

the effects of cushings syndrome on the body

A

cortisol levels are constantly higher than normal leading to:

severe muscle bone and skin breakdown

elevated glucose levels meaning high insulin levels, this targets adipocytes in the centre of the body and activates lipoprotein lipase which helps adipocytes accumulate- results in central obesity

hypertension due to amplified sensitivity to N and NA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

why does cushings cause sexual dysfunction

A

excess cortisol inhibits GnRH via negative feedback to the hypothalamus

this affects ovarian and testicular function, as this decreases FSH and LH from pituitary

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

what is the most common exogenous cause of cushings syndrome

A

steroid use

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

what is the most common endogenous cause of cushings syndrome

A

benign pituitary adenoma (known as Cushings disease)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
90
Q

for what type of cushings can metyrapone be used

A

for ACTH independant cushings

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
91
Q

how does metyrapone work

A

t inhibits hydroxylation in the adrenal cortex which decreases cortisol release (and to a lesser extent aldosterone)

this increases ACTH release from the pituitary, increasing the release of cortisol precursors (whilst inhibiting the enzymes requires to turn these into cortisol)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
92
Q

what are the consequences of having a bilateral adrenalectomy

A

body no longer produces glucorticoids (cortisol) or mineralocorticoids (aldosterone)

(therefore you need replacement therapy for them both)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
93
Q

when would someone who has has a bilateral adrenalectomy need to double their dose of glucorticoids

A

medical illness
physical/mental stress
trauma (including surgical procedure)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
94
Q

what is taken to replace cortisol

A

hydrocortisone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
95
Q

what is taken to replace aldosterone

A

fludrocortisone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
96
Q

what is primary adrenal insufficiency caused by

A

due to adrenocortical disease (doesn’t respond to ACTH)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
97
Q

what is secondary adrenal insufficiency

A

due to pituitary dysfunction (lack of ACTH, therefore adrenal glands not being stimulated)

98
Q

what is tertiary adrenal insufficiency caused by

A

due to hypothalamus dysfunction (lack of CRH)

99
Q

what is the survival rate of cushings syndrome if left untreated

A

50 percent after five years

100
Q

what percent of cushings is cushings disease

A

70 percent

101
Q

are more men or women affected by cushings disease

A

women 3:1

102
Q

most common age of onset of cushings disease

A

25-45

103
Q

which electrolyte disturbance may be seen in cushings

A

hypokalaemia

104
Q

are symptoms of cushings more easy to see in men or women typically

A

women (harder to detect cushings in men)

105
Q

in what other conditions would you see raised urinary cortisol

A

obesity
PCOS
depression

106
Q

what is the first screening tool used for cushings

A

salivary cortisol test

107
Q

what levels of ACTH would you see in ACTH dependant cushings

A

normal or raised

108
Q

what does low ACTH with cushings suggest

A

a primary adrenal cause

109
Q

which 2 clinical features suggest adrenal insufficiency

A

hypotension
hyponatraemia (low Na+)

if you see this treat for adrenal crisis straight away rather than awaiting bloods to see if serum cortisol and ACTH is low

110
Q

how to treat an adrenal crisis

A

high dose hydrocortisone

intravenous saline

111
Q

what does euvolemic mean

A

having the normal volume of blood in the body

112
Q

what is Addisons disease

A

inadequate secretion of the adrenal hormones (such as aldosterone and cortisol)

113
Q

what type of adrenal insufficiency is Addisons disease

A

primary adrenal insufficiency

114
Q

what are the 3 areas of the adrenal cortex

A

zona glomerulosa
zona fasiculata
zona reticularis

115
Q

what does the zona glomerulosa produce

A

mineralocorticoids (aldosterone)

116
Q

what does the zona fasiculata produce

A

glucocorticoids (cortisol)

117
Q

what does the zona reticularis produce

A

sex hormones
androgen precursors (DHEA)

118
Q

what is the most common cause of primary adrenal insufficiency in developed countries

A

autoimmune

119
Q

what is the most common cause of primary adrenal insufficiency in developing countries

A

tuberculosis (infection spreads from the lungs to the adrenal glands, destroying the adrenal cortex)

120
Q

symptoms of adrenal insufficiency usually present when what % of the adrenal cortex has even destroyed

A

90%

121
Q

what is the result of the zona glomerulosa being destroyed

A

hyperkalaemia
hyponatraemia
hypovolaemia
acidosis

122
Q

symptoms of zona glomerulosa being destroyed

A

cravings for salty food
nausea
vomiting
fatigue
dizziness

123
Q

what is the result of the zona fasiculata being destroyed

A

low blood glucose in times of stress

124
Q

symptoms of zona fasiculata being destroyed

A

weakness
tiredness
disorientation
hyperpigmentation especially at joints (due to negative feedback increasing the work of the pituitary)

125
Q

what is the result of the zona reticularis being destroyed

A

men are not affected as the testes are a big source of testosterone

women can experience loss of pubic and armpit hair and decreased sex drive

126
Q

what can trigger an addisonian crisis

A

injury
surgery
infection

there is a sudden need for aldosterone and cortisol

127
Q

presentation of addisonian crisis

A

pain in back, abdomen and legs

vomiting and diarrhoea leading to dehydration

low BP leading to loss of consciousness

128
Q

is addisonian crisis dangerous

A

yes can be fatal if left untreated

129
Q

which syndrome can trigger an addisonian crisis

A

waterhouse friderichsen syndrome

130
Q

how does waterhouse friderichsen syndrome cause an addisonian crisis

A

sudden increase in BP causes blood vessels in the adenal cortex to rupture

this fills the adrenal glands with blood causing tissue ischemia and adrenal gland failure

131
Q

how to diagnose Addisons

A

ACTH stimulation test
Synacthen test (same thing as above)

132
Q

how does the ACTH stimulation test work

A

synthetic ACTH is given

the cortisol and aldosterone produced is then measured

133
Q

treatment for Addisons disease

A

lifetime replacement of cortisol, aldosterone and androgens (hydrocortisone, fludrocortisone)

stopping can lead to addisonian crisis

134
Q

when would you do a cortisol 9am

A

to look for adrenal causes of symptoms

135
Q

why do you do haematinics for tiredness

A

to rule out iron, B12 and folate deficiency

136
Q

what the tests for non-specific symptoms of tiredness

A

bone profile- to rule out hypercalcaemia

haematinics

LFTs- to rule out chronic liver dysfunction

137
Q

typical presentation of Addisons disease

A

hyperpigmentation (bronze)

hypoglycaemia

changes in distribution of body hair

postural hypotension

GI disturbances

weight loss

weakness

extreme fatigue

138
Q

what pathology is related to the zona glomerulosa

A

conns syndrome

139
Q

what pathology is related to the zona fasiculata

A

cushings syndrome

140
Q

what pathology is related to the zone reticularis

A

congenital adrenal hyperplasia

141
Q

what does the adrenal medulla produce

A

adrenaline and noradrenaline

142
Q

what pathology is related to the medulla of the adrenal gland

A

phaeochromocytoma

143
Q

mechanism of action of metyraprone

A

it is a glucorticoid synthesis inhibitor

inhibits 11-beta-hydroxylase

this inhibits the formation of cortisol from deoxycortisol

also inhibits the formation of corticosterone from deoxycorticosterone

144
Q

treatment for addisonian crisis

A

IV hydrocortisone

IV 0.9% sodium chloride

145
Q

when is glucorticoid and mineralocorticoid therapy taken to mimic normal circadian rhythm

A

hydrocortisone 10mg on waking, 12pm and 4pm

fludrocortisone 100 microgram per day

146
Q

which gastrointestinal diseases can cause cough

A

gastro-oesophageal reflux

laryngo-pharyngeal reflux

147
Q

what would suggest viral illness with a cough

A

fever
sore throat
coryzal symptoms- these are the hallmark of upper respiratory tract symptoms including nasal stuffiness, runny nose, sneezing, sore throat

148
Q

what would suggest TB with a cough

A

recent foreign in travel
TB contacts
night sweats

149
Q

what would suggest asthma with a cough

A

history of eczema or hay fever
cough keeps them awake at night
associated breathlessness
wheeze
triggers such as perfumes

150
Q

what would suggest pneumonia with a cough

A

fever
coloured sputum
breathlessness

151
Q

what would suggest COPD with a cough

A

cough worse first thing in the morning
productive cough
smoker

152
Q

what would suggest bronchiectasis with a cough

A

history of copious sputum (large amounts of clear sputum)

153
Q

what would suggest lung cancer with a cough

A

haemoptysis
weight loss
smoker

154
Q

what would suggest post nasal drip with a cough

A

can feel a tickle at the back of their throat before they cough
nasal stuffiness/blocked nose
runny nose

155
Q

what would suggest gastro oesophageal reflux/laryngo pharyngeal reflux with a cough

A

cough worse after eating
heart burn

156
Q

what is a specific side effect of ACE inhibitors

A

dry cough

157
Q

why do ACE inhibitors cause dry cough

A

they increase bradykinin

usually occurs 1 week to 6 months after starting treatment

build-up of bradykinin irritates the airways causing inflammation and coughing

158
Q

which drugs can be given instead of an ACE inhibitor if the patient has experienced the dry cough side effect

A

angiotensin receptor blockers:

candesartan
irbesartan
losartan
valsartan

159
Q

hypervolemic causes of hyponatraemia

A

heart failure

cirrhosis

chronic kidney disease

nephrotic syndrome

160
Q

euvolemic causes of hyponatraemia

A

glucorticoid deficiency

hypothyroidism

SIADH (syndrome of inappropriate ADH secretion)- could be due to SCLC

mass lesions

inflammatory disease

degenerative demyelinating disorders

carcinoma of lung, prostate, larynx or pancreas

leukaemia

atypical pneumonia

COPD

AIDS related complex

drug induced

161
Q

hypovolemic causes of hyponatraemia

A

diuretic therapy

mineralocorticoid deficiency

third space loses

burns

pancreatitis

bowel obstruction

muscle trauma

salt wasting neuropathy

vomting and diarrhoea

cerebral salt wasting syndrome

sweat losses

162
Q

what tests to do if someone is euvolemic but has hyponatraemia

A

plasma osmolarity

cortisol

thyroid function

urinary sodium and osmolarity

163
Q

when should a cough be investigated via chest X-Ray

A

if over 4 weeks

164
Q

what are sodium levels like if plasma osmolarity is increased

A

Na levels are increased

165
Q

increased sodium makes you feel what

A

triggers hypothalamus
makes you feel thirsty

166
Q

increased sodium prompts the release of what

A

ADH (vasopressin)

167
Q

what does ADH do?

A

acts on the collecting ducts of the kidneys to increase the number of aquaporin channels

this allows for water to be absorbed into the blood (increases BP)

168
Q

is diabetes insipidus common

A

rare

169
Q

pathophysiology of diabetes insipidus

A

either too little ADH is produced by the pituitary (cranial diabetes insipidus)

or

the kidney becomes insensitive to ADH and so does not insert aquaporins to reabsorb water from collecting ducts (nephrogenic diabetes insipidus)

170
Q

what are the clinical manifestations of diabetes insipidus

A

large amounts of dilute urine are produced- polyuria

excessive thirst- polydipsia

nocturia

171
Q

what happens if those with diabetes insipidus are not able to drink water

A

hypernatraemia
dehydration

172
Q

diagnosis of diabetes insipidus

A

water restriction test urinalysis

173
Q

what is the normal amount of urine to urinate per day

A

1-3 litres

174
Q

how much urine do those with diabetes insipidus urinate

A

19L

175
Q

risk factors for diabetes insipidus

A

FH
diuretics
low calcium and hyperkalaemia
serious head/brain injury

176
Q

what is SIADH

A

syndrome of inappropriate antidiuretic hormone

high amounts of ADH are inappropriatly released

this causes the reabsorption of water from the collecting ducts

means high sodium in urine but hyponatraemia in blood

177
Q

diagnosis of SIADH

A

comparison of urinary and serum sodium

serum osmolarity is low whereas urinary osmolarity is high

178
Q

causes of SIADH

A

lung diseases- cancer, pneumonia

brain lesions- tumour, head injury and bleed, stroke

drugs- carbamazepine, SSRIs

179
Q

when to suspect psudeohyponatraemia

A

this is a laboratory error if there are high levels of glucose, lipids, protein or urea

serum osmolarity will be norma

180
Q

symptoms of true hyponatremia

A

headache
nausea
dizziness
severe can result in coma

181
Q

what status of the patient should you check with hypoatraemia

A

hydration status

182
Q

signs of dehydrated/hypovolaemic hyponatraemia

A

cool peripheries

prolonged capillary refil

tachycardia

weak thread pulse

postural hypotension

confusion

dry mucus membranes

reduced skin turgor

183
Q

signs of fluid overloaded/hypervolaemic hyponatraemia

A

tachycardia

bounding pulse

raised JVP

pulmonary oedema/pleural effusions

ascites

peripheral oedema

184
Q

most common causes of hyperatraemia

A

only associated with dehydration where the person has been unable to access water:

elderly with dementia
medically induced comas
hot weather (desert)

185
Q

treatment of SIADH

A

fluid restriction (1.5 litres per day)

hypertonic saline

demeclocycline

186
Q

common causes for abdominal distention

A

fetus

fluid- ascites

feces- sub-acute intestinal obstruction/constipation

flatus

fat- obesity

distended bladder

abdominal mass- neoplasm, hernia, aortic anyeurysm

organomegaly- kidneys, liver, spleen

187
Q

what is the major complication of hernias

A

intestinal obstruction/strangulation

188
Q

what 2 conditions can cause peripheral oedema and ascites

A

nephrotic syndrome
congestive heart failure

189
Q

what conditions cause hepatomegaly

A

hepatic steatosis

alcoholic liver disease

viral hepatitis

primary biliary cirrhosis

right heart failure

secondary metastatic cancer

primary hepatocellular cancer

190
Q

what conditions cause splenomegaly

A

glandular fever

portal hypertension

haemolytic anaemia

rheumatoid arthritis (Feltys syndrome)

systemic lupus erythematosus

malaria, kala-azar (leishmaniasis)

brucellosis, tuberculosis, salmonellosis

bacterial endocarditis

191
Q

what causes both hepatomegaly and splenomegaly

A

leukaemia

lymphoma

myelofibrosis

polycythaemia

192
Q

how do the kidneys descend on inspiration

A

vertically down

193
Q

what do the kidneys feel like on palpation

A

smooth and regular in shape (enlarged polycystic kidneys have an irregular shape)

194
Q

what on palpation would suggest you are palpating the spleen

A

palpable notch on the medial surface

195
Q

what does shifting dullness suggest on examination

A

ascites

196
Q

causes of ascites

A

hypoalbuminaemia- nephrotic syndrome

hepatic cirrhosis with portal hypertension

intra-abdominal malignancy with peritoneal spread

constructive pericarditis with right heart failure

197
Q

what on urine dipstick suggests nephrotic syndrome

A

proteinuria

198
Q

what be seen on urine dip with nephritic syndrome

A

++ blood
++ protein

199
Q

what be seen on urine dip with UTIs and renal stones

A

++ blood
++ nitrates
++ leukocytes

200
Q

what be seen on urine dip with nephrotic syndrome

A

+++ protein

201
Q

what be seen on urine dip with menstrual cycle, anti-platelet therapy and malignancy of the kidney, ureter or bladder

A

+++ blood

202
Q

what are mild nephritic syndromes usually associated with

A

inflammatory lesions of the glomeruli on light microscopy (focal glomerulonephritis)

203
Q

what is seen with mild nephritic syndrome in urine

A

mild proteinuria

204
Q

symptoms of advanced nephritic syndrome

A

heavy proteinuria
oedema
hypertension
kidney function impairment

205
Q

triad of findings with nephrotic syndrome

A

heavy proteinuria
hypoalbuminaemia
peripheral oedema

206
Q

what other findings may be seen with nephrotic syndrome

A

hyperlipidaemia
thrombotic disease

207
Q

difference between nephrotic and nephritic syndrome on urine dip

A

nephritic syndrome= blood and protein in urine

nephrotic= protein in urine

208
Q

what may back/flank pain suggest

A

renal cancer
renal stone
acute pyelonephritis
APKD
nephrotic syndrome
nephritic syndrome

209
Q

what may lower limb oedema suggest

A

nephritic syndrome
nephrotic syndrome
APKD

210
Q

prenreal causes of AKIs

A

renal stone
acute pyleonephritis
APKD
nephrotic syndrome

211
Q

renal causes of AKIs

A

nephritic syndrome
nephrotic syndrome

212
Q

postrenal causes of AKIS

A

renal stones

213
Q

what is the consequence of dehydration on osmolality

A

it increases osmolality

214
Q

where is ADH produced

A

hypothalamus (the supra optic nucleus)

215
Q

the issues with diabetes insipidus is in either of which two places

A

hypothalamus
kidneys

216
Q

treatment of diabetes insipidus

A

for central and gestational- desmopressin (ADH analogue which acts like ADH)

for nephrogenic- thiazide diuretics to increase the urinary excretion of sodium

217
Q

what is the cause of gestational diabetes insipidus

A

release of vasopressinase by the placenta

218
Q

what is nephrotic syndrome

A

there is an issue with podocytes (or basement membrane)of the glomerulus meaning they are not able to keep the protein in
as a result, there is a loss of protein

219
Q

what does protein in the urine look like

A

frothy

220
Q

what protein is lost the most with nephrotic syndrome

A

albumin

221
Q

why can you see increased lipids with nephrotic syndrome

A

the liver compensates with lipids for the loss of albumin

there is increased lipids in urine and blood

222
Q

why can there be thrombosis with nephrotic syndrome

A

there is loss of antithrombin-III (AT-III) in the urine

this leads to poor anticoagulation

can see thrombosis particularly in the renal veins (can also have DVT and PE)

223
Q

what is nephritic syndrome

A

there is glomerular inflammation due to complexing forming

WBCs are recruited

this allowed for WBCs, proteins and RBCs to seep through basement membrane and podocytes (they cant usually do this)

224
Q

how is urination affected by nephritic syndrome

A

oliguria- decreased urination (due to the damaged glomerulus not being able to filter properly)

225
Q

how is BP affected by nephritic syndrome

A

hypertension

226
Q

3 most common causes of nephrotic syndrome

A

focal segmental glomerulosclerosis (FSGS)

minimal change disease

membranous nephropathy

227
Q

causes of nephritic syndrome

A

membranoproliferazive glomerulonephritis (MPGN)

ANCA vasculitis

good pastures disease

crescentic glomerulonephritis

oliguria

228
Q

treatment of crescentic glomerulonephritis

A

aggressive steroids

229
Q

what is the gold standard for diagnosing nephritic and nephrotic syndrome

A

renal biopsy (under ultrasound)

230
Q

what type of disease is APKD

A

autosomal dominant

231
Q

aside from renal, what other abnormalities is APKD associated with

A

hepatic and cardiovascular

232
Q

pathophysiology of APKD

A

there is mutation of polycystin (this is responsible for sensing flow in the tubule

disruption results in decreased cytoplasmic calcium which in the principal cells of the collecting duct causes disorientated cell division leading to cyst formation

233
Q

at what age do the presenting symptoms of APKD typically manifest

A

from the second decade onwards

234
Q

what are some of the presenting symptoms of APKD

A

loin pain and/or haematuria from haemorrhage into a cyst, cyst infection or urinary tract stone formation

loin/abdominal discomfort as size of kidneys increase

subarachnoid haemorrhage associated with berry aneurysm rupture

complications of hypertension

complications of associated liver cysts (occurs in 50%)

symptoms of uraemia and/or anaemia associated with CKD

235
Q

potential strategy for management of APKD

A

vasopressin receptor antagonists- they inhibit cAMP in principal cells, reduce cyst growth and slow the progression of renal failure

are used in those with eGFR less than 30 with rapid disease progression

236
Q

what does anti-PLA2R-ab antibody test for

A

primary membranous nephropathy

237
Q

overall management of nephrotic syndrome

A

salt restriction

fluid restriction

diuretics

ACE inhibitors/angiotensin receptor blockers

atorvastatin

anticoagulation

238
Q

when do you take orlistat

A

before each meal

239
Q

when must you stop taking orlistat

A

if 5% of total body weight has not been lost in the first 12 weeks patient must stop taking orlistat and consider other weight loss options

240
Q

which test allows for discrimination between pituitary and ectopic causes of excess ACTH

A

inferior petrosal sinus samling

241
Q

what criteria must you meet on ultrasound to diagnose APKD with a positive family history

A

must be 15-29 years old with 3 or more cysts bilaterally

Semester 1 ( 3rd Year) (12 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions