Block 32 Week 8 Flashcards
1
Q
acute pancreatitis?
A
- acute inflammation of the pancreas
- uncontr release of activated pancreatic enzymes -> autodigestion
2
Q
most common cause of acute panc?
A
1) Gallstones
2) alcohol
3
Q
I GET SMASHED
A
4
Q
gallstones -> panc?
A
- most common cause
- almost half of cases
- can obstruct the ampulla -> biliary reflux
5
Q
alcohol -> acute panceatitis?
A
- increased production of digestive enzymes
- alcohol commonly causes chronic panc but also causes acute
6
Q
ERCP?
A
-> acute panc
7
Q
endocrine function of pancreas?
A
- islets of langerhans
- insulin and glucagon
8
Q
exocrine function of panc?
A
- pancreatic ductal cells
- produce pancreatic juice
- trypsin imp in pancreatitus
9
Q
pain in acute panc?
A
- sudden onset epigastric pain
- vomiting
- worse on movement
- radiation to back
10
Q
why may patients have reduced urinary output in panc?
A
- vomiting and third spacing of fluid - fluid exits the vascular space into tissues due to inflammation
- can result in a significant fluid deficit and as such patients may have dry mucous membranes and reduced urinary output
11
Q
Sx of acute panc?
A
- Abdominal pain (may radiate to the back)
- Nausea
- Vomiting
- Anorexia
- Diarrhoea
12
Q
Signs of acute panc?
A
- Abdominal tenderness
- Abdominal distention
- Tachycardia
- Tachypnea
- Pyrexia
13
Q
Acute panc - 2 signs?
A
Cullens sign and grey turners
14
Q
Cullens sign =
A
peri-umbilical bruising
15
Q
grey turner sign?
A
flank bruising
16
Q
diagnostic test of acute panc?
A
amylase 3x the reference range
17
Q
how long does amylase stay elevated?
A
- 3 days
- patients who present late may have a missed peak
18
Q
amylase in acute on chronic panc?
A
even in severe pancreatitis the amylase may be normal, particularly in those with acute-on-chronic disease. In these cases, a CT abdomen and pelvis is generally needed to confirm the diagnosis and exclude alternative causes.
19
Q
mild elevation of amylase?
A
- parotitis
- bowel obstruction
- intestinal inflammation
- trauma
- malignancy
- ruptured ectopic pregnancy
20
Q
Lipase vs amylase?
A
- lipase is more specific for panc
- has a longer half life so levels remain elevated for longer
21
Q
lipase levels suggesting acute panc?
A
3x above reference range
22
Q
bedside Ix for acute panc?
A
- Observations
- ECG
- Blood sugar
- Pregnancy test
23
Q
Bloods for panc?
A
- amylase/ lipase
- U&Es
- LFTs - assessing for cholangitis
- LDH
- glucose
- lipids
24
Q
US in acute panc?
A
used to demonstrate gallstones or a dilated common bile duct. The pancreas may be visualised.
25
CT in acute panc?
used to confirm diagnosis when uncertainty remains and to exclude complications of disease.
26
MRCP in acute panc?
most commonly indicated in suspected gallstone pancreatitis to help evaluate for CBD stones.
27
scoring for acute panc?
glasgow
28
glasgow score indicating severe panc?
> 3
29
Tx of acute panc?
- supportive
- IV fluids
- Analgesia
- Nutritional support
30
nutrition in acute panc?
in mild cases low fat diet reintro
31
Severe panc - feeding?
- enteral feeding is preferred to total parenteral nutrition (TPN).
- It is thought enteral feeding helps maintain the mucosa and prevents translocation of bacteria. Nasojejunal feeding is commonly used.
32
when should ab be used?
- NOT for acute panc
- should be used for suspected cholangitis
33
ERCP?
- Gallstone panc
- stone extraction
34
pancreatic necrosis?
- continued inflammation -> local thrombosis, haemorrhage and necorsis in the panc
- high infection risk
- major cause of mortality
35
Ix for pancreatic necrosis?
- CT guided fine needle aspiration and culture
36
panc pseudocyst?
- present 4+ weeks after an episode
- psudo means epithelial lining around the cyst rather than granulation tissue
37
vascular complications of acute panc?
- pseudoaneurysm
- venous thrombosis
38
pseudoaneurysm?
- rare but life threatning haemorrhages
- often seen in splenic and hepatic arteries
- normally occur in association w pancreatic pseudocysts
39
venous thrombosis?
- venous thrombosis may affect the portal, splenic and superior mesenteric veins
- requires AC
40
Severe acute pancreatitis can lead to ->
- Acute respiratory distress syndrome
- Renal failure
- Shock - disrtibutive
41
mortality in acute panc?
- 1% in mild panc
- sterile pancreatic necrosis: 10%
- infected panc necrosis: 25% mortality
42
Chronic pancreatitis refers to
chronic, irreversible, inflammation and/or fibrosis of the pancreas.
43
leading cause of chronic panc?
alcohol
44
endocrine dysfunction in chronic panc?
Endocrine dysfunction: damage to the islet cells result in lack of insulin and development of diabetes mellitus
45
exocrine dysfunction in chronic panc?
Exocrine dysfunction: damage to the acinar cells results in lack of pancreatic enzymes and malabsorption
46
Classification of the causes of panc?
TIGAR-O
47
Tigar-O?
T (toxic/metabolic): alcohol, smoking, high triglycerides, hypercalcaemia, chronic kidney disease
48
tIgar-O?
- idiopathic
- may be late onset, early onset or tropical
49
tiGar-O?
- genetics
- mutation in PRSS1
50
autoimmune panc?
- type 1
- type 2
51
Type 1 autoimmune panc?
- IgG4 disease
52
Type 2 autoimmune panc?
limited to the pancreas and associated with inflammatory bowel disease
53
tigaR-O?
- recurrent and severe acute panc
- patients with a severe episode of necrotising pancreatitis or those with acute recurrent pancreatitis can progress to chronic pancreatitis due to tissue destruction
54
tigar-O?
- chronic obstruction of the main pancreatic duct can lead to tissue damage and chronic pancreatitis upstream.
- Typical causes of obstruction include strictures, stones, cysts, and tumours
55
autosomal dominant hereditary panc?
- PRSS1 mutation
- encodes cationic trypsinogen
56
autosomal recessive hereditary panc?
- mutation in CTFR gene
- spink 1 gene
57
most common feature of chronic panc?
abd pain
58
pain in chronic pain?
- epigastric discomfort
- worse post-prandially and on lying down
59
pain in chronic panc may be assoc w ?
- nausea
- vomiting
- anorexia
60
CP - exocrine insufficiency?
- destruction of acinar cells -> loss of digestive enzymes -> malabs
- inability to digest fatty foods due to lack of lipase
61
features of panc exocrine insufficiency?
- Weight loss
- Bloating
- Flatulence
- Abdominal pain/discomfort
- Loose stools
- Steatorrhea
- > 90% of the pancreatic exocrine function needs to be lost before patients develop steatorrhea - consq of long standing panc damage
62
loss of endocrine cells in CP?
- Type 3c DM
- Polyuria, polydispsia, weight loss
63
assessment of chronic panc?
- CT or MRI with MRCP
64
features of chronic panc on CT?
- CT is excellent at looking for calcification changes within the pancreas.
- Features of chronic pancreatitis include atrophy, calcification, and ductal changes (e.g. dilatation, strictures).
65
Fecal elastase?
- indirect marker of panc function
- used to assess for panc exocrine insufficiency
- low levels suggest PEI
66
Bloods in CP?
- FBC, U&Es, LFTs
- lipid profile
- bone profile
- mag
- hbalc
67
general management of chronic panc?
- nutritional assessment
- alcohol cessation
- smoking cessation
- vitamin replacement e.g. vitamin D
68
Pain relief in chronic panc?
- basic first: paracetamol and NSAIDs
- then weak opiods: tramadol, codeine
69
PEI management?
- pancreatic enzyme replacement therapy
- abs can be improved using a PPI
70
Endoscopic management for chronic panc when:
- Pancreatic pseudocysts
- Pancreatic stones
- Main pancreatic duct strictures
- Other complications (e.g. biliary strictures,
duodenal obstruction)
71
complications of chronic panc?
- PEI
- DM
- osteoporosis
- panc cancer
- duodenal and biliary obst
72
Hb ab interpretation?
HBsAg = ongoing infection, either acute or chronic if present > 6 months
anti-HBc = caught, i.e. negative if immunized
73
Transmission of hep A?
- faecal-oral
74
hep A disease coruse?
- self limiting
- doesn't cause chronic disease
75
features of hep A?
* flu-like prodrome
* abdominal pain: typically right upper quadrant
* tender hepatomegaly
* jaundice
* deranged liver function tests
76
immunisation for hep?
- A
- B
77
hep B is a
double standed DNA hepadanvirus
78
how is hep B spread?
- exposure to infected blood or body fluids
- mother to child
79
incubation period for hep B?
6-20 weeks
80
features of hep B?
- fever
- jaundice
- elevated LFTs
81
features of chronic hep B on LM?
ground glass hepatocytes
82
complications of hep B
- HCC
- glomerulonephritis
- fulm liver failure
83
hep E spread?
- faecal oral
- Can be transmitted by seafood
84
incubation period of hep E?
3-8 WEEKS
85
Where is hep E common?
- central and south asia
- mexico
- north and west africa
86
hep E is especially problematic in?
- pregnancy - causes sig mortality
87
hep E does not cause ?
does not cause chronic disease or an increased risk of hepatocellular cancer
88
hep C affects?
- IV drug users
- patients who receive a blood transfusion
89
incubation period of hep C?
6-9 weeks
90
transmission of HepC?
- Needle stick injury
- mother to child
- sexual intercourse
91
what is not contra-indicated in hep C?
breastfeeding
92
there is no vaccine for ?
hep C
93
Comps of chronic hep C?
- Sjogren's syndrome
- cirrhosis
- HCC
- glomerulonephritis
94
hep D?
- single stranded RNA virus
- transmitted parenterally (blood and body fluids)
95
how does hep D cause infection?
- requires hep B surface antigen to repllicate
96
how is hep D transmitted?
transmitted in a similar fashion to hepatitis B (exchange of bodily fluids) and patients may be infected with hepatitis B and hepatitis D at the same time.
97
Co-infection vs superinfection?
Co-infection: Hepatitis B and Hepatitis D infection at the same time.
Superinfection: A hepatitis B surface antigen positive patient subsequently develops a hepatitis D infection.
98
superinfection of hep B and D is assoc w a higher risk of?
Superinfection is associated with high risk of fulminant hepatitis, chronic hepatitis status and cirrhosis.
99
Ascending cholangitis is?
- infection of the biliary ducts
- caused by obstruction
100
how does ascending cholangitis present?
Charcots triad: fever, jaundice, RUQ pain
101
Reynol'd pentad?
- Ascending cholangitis
- fever, jaundice, RUQ pain, septic shock and mental confusion
102
common causes of asc cholamgitis?
choledocholithiasis (gallstones) and strictures of the biliary tree.
103
Reynold's pentad indicated?
inc risk of septic shock -> medical emergency
104
LFTs with Ascending cholangitis?
hyperbilirubinaemia and elevated serum alkaline phosphatase
105
imaging for Ascending cholangitis?
- ERCP: when history of biliary disease
- transabd US: CBD dilatation
106
Mx of ascending cholangitis?
- pieracillin/ tazobactam
- IV fluids
- analgesia
- sepsis 5
107
definitive management of ascendinh cholngitis?
- biliary decompression
- ERCP or surgery
108
biliary colic pain?
- RUQ pain
- intermittent
- usually begins abruptly and subsides gradually
- attacks often occur after eating
109
Biliary colic - mneumonic?
- female
- forties
- fat
- fair
110
Acute cholesystitis pain?
- similar to biliary colic but more severe and persistent
- pain may radiate to back or right shoulder
111
acute cholesytitis sign?
- pyrexial
- murphy's sign positive: arrest of inspiration on palpation of the RUQ
112
Gallstone ileus?
- SBO
- secondary to impacted gallstone
113
features of gallstone ileus?
Abdominal pain, distension and vomiting
114
Features of cholangiocarcinoma?
- persistent biliary colic symptoms
- anorexia
- jaundice
- weight loss
115
Signs of cholangiocarcinoma?
- Courvoiser's sign
- sister mary joseph nodes
- virchow node
116
Courvoisier sign?
palpable mass in the right upper quadrant
117
Sister mary joseph nodes?
periumbilical lymphadenopathy
118
virchow node?
left supraclavicular adenopathy
119
acute panc pain is usually due to?
alcohol or gallstones
120
features of acute panc pain?
- Severe epigastric pain
- Vomiting is common
- Examination may reveal tenderness, ileus and low-grade fever
121
pancreatic cancer features?
- painless jaundice
- anorexia
- weight loss
122
differentiating pain
* Biliary colic --> pain
* Acute cholecystitis --> pain + fever
* Ascending cholangitis --> pain + fever + jaundice
123
Mirrizi syndrome?
In Mirizzi syndrome the stone may compress the bile duct directly- one of the rare times that cholecystitis may present with jaundice
124
infection in cholangitis is due to?
E coli
125
Panc cancer?
Typically painless jaundice with palpable gallbladder (Courvoisier's Law)
126
cholangiocarcinoma is linked to
PSC
127
RF for gallstones?
- Fat
- Female
- Fertile - pregnancy
- Forty
128
Other RF for gallstones?
- diabetes
- chrons
- rapid weight loss
- drugs - fibrates, oral contraceptive
129
Features of gallstones?
- colicky right upper quadrant abdominal pain worse postprandially, worse after fatty foods
- the pain may radiate to the right shoulder/interscapular region
- N and V
130
distinguishing biliary colic from other gallstone related conditions?
in biliary colic there is no fever and liver function tests/inflammatory markers are normal
131
choledocholithiasis=
gallstones in common bile duct
132
cholelithiasis =
Cholelithiasis (gallstones) refers to the development of a solid deposit or ‘stone’ within the gallbladder.
133
who do gallstones tend to affect?
They are more common in women and tend to affect those of caucasian, Native American and hispanic backgrounds more.
134
RF for gallstones?
- age
- female
- obesity
- rapid weight loss/ prolonged fasting
- diabetes
- crohns
135
medications linked to gallstones?
oestrogen replacement therapy, ceftriaxone, octreotide
136
CF of gallstones?
- intermittent RUQ/ epigastric pain
- nausea and vomiting
137
Ix for gallstones?
- USS - can also assess for CBD dilation
- LFTs
138
symptomatic management of gallstones?
- analgesia - paracetamol and NSAIDs
- diet - low fat
139
surgical management of gallstones?
- elective cholecystectomy
140
cholethiasis refers to?
Cholelithiasis (gallstones) refers to the development of a solid deposit or ‘stone’ within the gallbladder.
141
Choledocholithiasis =
gallstones within the biliary tree.
142
biliary colic =
refers to a self-limiting pain in the RUQ/epigastrum associated with gallstones.
143
acute cholecystitis =
refers to the acute inflammation of the gallbladder, most commonly caused by gallstones.
144
acute cholangitis =
refers to the acute inflammation of the gallbladder, most commonly caused by gallstones.
145
cholesterol stones?
- most common type
- occur due to crystalisation of cholesterol in bile due to supersaturation of cholesterol
146
black pigment stones?
- dark stones composed primarily of calcium bilirubinate
- They occur in people with increased amounts of bilirubin in their bile - hyperbilirubinbilia
- occurs w inc haemolysis
147
brown pigment stones?
- mix of calcium bilirubinate and a calcium salts of fatty acids
- mostly occur in association with infection
148
comparison of abd pain?
149
biliary colid observations?
- normal
- BTs normal
150
acute cholesystitis symptoms?
RUQ pain, fevers, malaise
151
observations of acute cholesytitis?
- fever
- haemodynamic instability
152
examination in acute cholesystitis?
- tenderness
- localised guarding may be present
153
USS of acute cholesystitis?
- gallstones
- inflamed, thickened GB
- pericholesytitic fluid
154
acute cholangitis obs?
fever and haemodynamic instability
155
acute cholangitis features?
- jaundice
- tenderness
156
acute cholangitis findings on US?
CBD stone, duct dilatation
157
acute panc summary?
- epi pain radiating to back
- fever and tachy
- epigastric tenderness
- raised amylase
158
Prostate cancer should be suspected in people who have any of the following symptoms that are unexplained:
- Lower back or bone pain.
- Lethargy.
- Erectile dysfunction.
- Haematuria.
- Anorexia/weight loss.
- Lower urinary tract symptoms (LUTS), such as frequency, urgency, hesitancy, terminal dribbling, and/or overactive bladder.
159
Which anti-glycaemic drugs can be used to reduce CVD events, kidney failure and heart failure hospitalisation?
- SGLT2 inhibitors: cardiovascular and renal benefits - e.g. CREDENCE trial
- GLP-1 analogues -> CV benefit
160
ppl w diabetes experience high rates of?
people with diabetes experience disproportionately high rates of mental health problems such as depression, anxiety and eating disorders.
161
diabulimia?
- diabulimia involves the deliberate manipulation of insulin doses to control weight -> poor glycaemic control and ketosis
162
MH problems in diabetes?
- Diabetes disress - constant vigilance -> stress
- depression and anxiety - stress of a chronic condition, stress about a hypo
- increased risk of EDs - condition called diabulimia
- Chronic hyperglycemia and fluctuations in blood sugar levels can affect cognitive function in individuals with type 1 diabetes
163
disordered eating in diabetes may be due to?
- Insulin omission/ manipulation
- Fear of hypos -> restrictive eating
- Food rules and rituals - only eating at certain times and developing strict meal plans
- Body image concerns - focus on weight
164
main interventions to reduce CV morbidity and mortality in T1D - CV risk assessment?
- eGFR and ACR
- Smoking
- BP control
- full lipid profile
- age
- FHx of CVD
- abd adiposity
165
Interventions to reduce risk and manage CVD - T1D?
- Stop smoking
- BB for those who have had a stroke or MI
166
Offer statin treatment for the primary prevention of CVD to adults with type 1 diabetes who:
- are older than 40 years or
- have had diabetes for more than 10 years or
- have established nephropathy or
- have other CVD risk factors.
167
Consider ? Treatment in T1D for CVD prevention
Consider statin treatment for the primary prevention of CVD for people aged 18 to 40 with type 1 diabetes, including those who have had diabetes for 10 years or less.
168
the role of transplant in t1d?
- for adults w T1D who have recurrent severe hypoglycaemia that has not responsed to other treatments
- consider referral to for islet and/or pancreas transplantation
- Consider islet or pancreas transplantation for adults with type 1 diabetes with suboptimal diabetes control, if they have had a renal transplant and are currently on immunosuppressive therapy.
169
appetite control centre is in the?
- in the hypothalamus
- arcuate nucleus -> appetite controle
170
excitatory vs inhibitory NTs?
- Excitatory neurons release NPY -> hunger
- Inhibitory neurons release -> POMC
171
ghrelin?
- Ghrelin is a peptide hormone produced in the pancreas and released from the stomach wall when the stomach is empty.
- This stimulates the excitatory primary neurones, and therefore stimulates appetite. When the stomach is full, ghrelin release is inhibited, thus the appetite stimulus is also inhibited
172
PPY?
from the ileum in response to feeding. Causes appetite suppression
173
Leptin?
- leptin is produced by fat cells
- stimulates inhibitory neurones and inhibits excitatory neurons in the arcuate nucleus -> appetite suppression
174
Insulin?
- Insulin is a hormone released from beta cells in the islets of Langerhans of the pancreas. This suppresses appetite in a similar way to leptin.
175
How does the stomach signal to the brainstem?
vagus nerve
176
How do we detect that we're hungry?
- Empty stomach senses by stretch receptors in the stomach -> signal to BS
- Ghrelin -> arcute nucleus of hypothalamus
- Ghrelin -> paraventicular nucleus to increase food intake and decrease energy expenditure
177
Stomach distension?
- distension of stomach stops ghrelin production
- Gut peptides like GLP-1 and CCK are released which then act on the BS and hypothalamus
- suppressing appetite and increasing energy expenditure
178
LT metabolism regulation?
- High fat -> stop feeding and spend energy
- Low fat -> feed more, preserve more energy
179
Leptin release is dependent on?
- Leptin release is dependent on insulin and is released from adipose tissue
- Increased leptin -> stop eating and spend energy
- Inhibit food intake at hypothalamus
180
Obesity results from?
- results from disregulation of this system
- assoc w chronic low leptin - makes the body think its starved which leads to obesity
181
Lifestyle in obesity development?
- high fat diet -> saturated fats -> inflammation -> leptin resistance -> starvation response
- Leptin deficiency or mutations leading to leptin resistance
182
Roles of insulin?
- Insulin -> GLUT4 insertion -> glucose enters cell
- Causes glycogen production, inhibits glucogonegenesis
183
Roles of glucagon?
- Glucagon - released when all the glucose
- inactivates glycogen synthesis
- inc glucogenolysis
- Adrenaline acts the same as glucagon but faster
184
Roles of BMI?
- screening tool - quick and easy way to assess weight
- health risk assessment - Individuals with higher BMI values are generally at increased risk of developing these conditions compared to those with lower BMI values.
- population health monitoring
- clinical decision making
185
-Limitations of BMI
- Doesn't distinguish between fat and lean body mass
- not applicable to different age and ethniticities
- BMI does not account for distrubution of body fat
- not suitable for pregnancy
186
classification of obesity?
- healthy weight: BMI 18.5 kg/m2 to 24.9 kg/m2
- overweight: BMI 25 kg/m2 to 29.9 kg/m2
- obesity class 1: BMI 30 kg/m2 to 34.9 kg/m2
- obesity class 2: BMI 35 kg/m2 to 39.9 kg/m2
- obesity class 3: BMI 40 kg/m2 or more
187
Waist circumference indicating obesity?
Men: ≥ 102 cm (40 inches)
Women: ≥ 88 cm (35 inches)
188
lifestyle Ix of obesity?
- dietary changes - lifestyle interventions
- reducing calories
- increasing fruit and veggies
- physical activity
- behavioural strategies - goal setting, self monitoring
- education - nutrition, exercise. weight management
189
Limitations of lifestyle Ix in obesity?
- complexity of disease - multifactorial so won't address underlying genetic factors
- indiv variability
- sustainability - challenging to do long term
190
Psych factors in using lifestyle Ix in obesity?
Emotional eating, stress, depression, and other psychological factors can undermine efforts to adopt healthier lifestyles. Lifestyle interventions may need to incorporate strategies to address these psychological barriers effectively.
191
when is bariatric surgery indicated in obesity?
BMI > 40
192
Least restrictive bariatric surgery?
LABG
193
LABG
- least restrictive
- first line
- less weight loss but less comps
194
What does a sleeve gastrectomy do?
reduces size of stomach
195
What does the duodenum abs?
= Metal ions + Folate (first)
196
Jejenum vs ileum abs?
- Jejunum = all vitamins except
- Ileum = B12
197
What does the LI abs?
Na, K, water
198
Initial Ix of Pituitary disease?
- ACTH
- FSH/ LH
- TSH
- GH
- prolactin
199
pathophys of thyroid eye disease?
- autoimmune response against an autoantigen, possibly the TSH receptor → retro-orbital inflammation
- the inflammation results in glycosaminoglycan and collagen deposition in the muscles
200
RF for Thyroid eye disease?
- most imp: smoking
- radiodine treatment - predinoslone can reduce risk
201
CF of thyroid eye disease?
- the patient may be eu-, hypo- or hyperthyroid at the time of presentation
- exophthalmos
- conjunctival oedema
- optic disc swelling
- ophthalmoplegia
- inability to close the eyelids may lead to sore, dry eyes. If severe and untreated patients can be at risk of exposure keratopathy
202
Mx of thyroid eye disease?
- smoking cessation
topical lubricants may be needed to help prevent corneal inflammation caused by exposure
- steroids
- radiotherapy
- surgery
203
thyroid issues in the pregnancy/ post-partum period?
- the typical symptoms of pregnancy often emulate symptoms of thyroid dysfunction, creating a significant diagnostic challenge during this time
- during pregnancy, thyroid gland enlarges and TFTs change - T3 and T4 increases but TSH decreases
204
TFTs in pregnancy?
- due to human chorionic gonadotropin (hCG) cross-reacting with TSH receptors; total T4 (TT4) levels increase while free T4 (FT4) levels remain unchanged.
205
Roles of meds in causing thyrotoxicosis?
amiodarone and immune checkpoint inhibitors in causing thyroid hormone excess
206
Subclinical hyperthyroidism TFTs?
- normal T3 and T4 levels
- TSH is low (suppressed)
207
Causes of subclin hyperthyroidism?
MNG paticularly in elderly females
208
Problems in subclinical hyperthyroidism?
- AF
- osteoporosis
209
Mx of subclinical hyperthyroidism?
- TSH levels often revert to normal - therefore levels must be persistently low to warrant intervention
- a reasonable treatment option is a therapeutic trial of low-dose antithyroid agents for approximately 6 months in an effort to induce a remission
210
Subclinical hypothyroidism TFTs?
TSH raised T3 and T4 normal
211
Significance of subclin hypothyrodisim?
- risk of progressing to overt hypothyroidism - higher in men
- risk increased by presence of thyroid autoantibodies
212
Mx of subclin hypo?
- TSH >10 -> levothyroxine
213
What is an adrenal incentaloma?
- Incidentaloma - mass found upon imaging
- was not carried out for sus of adrenal disease
214
Signs and symptoms of adrenal incidentaloma?
- usually no typical findings
- mild autonomous cortisol excess
215
sig of an adrenal incidenataloma?
- Have an increased incidence of metabolic disease like T2DM, HTN, osteoporosis, dyslipidemia
216
Ix for an adrenal incidentaloma?
- CT for diagnostic uncertainty on whether it's a cancer
- Urine metanephrines
- > 4cm mass requires urgent assessment for malignancy
217
Other Ix of adrenal incidentaloma?
- Glucocorticoids - Dexamethasone suppression test
- Urine and plasma metanephrines
218
Mx of an adrenal incidentaloma?
- Benign and no hormone excess -> no follow up
- Clinically overt cortisol excess or aldosterone or catecholamines -> surgery?
219
site of origin for a phaechromocytoma?
- chromaffin cells of the adrenal medulla -> catecholamine hypersecretion
- may also develop at extra-adrenal sites -> paraganlionomas
220
Triad for phaechromocytoma?
episodic headache, diaphoresis, and tachycardia
221
Diagnosis of phaechrocytoma?
- Plasma or urinary fractioned metanephrines
- Followed by CT/ MRI for localisation
222
# associations
Pathophys of Phaechromoytoma?
- MEN11 association
- Von Hippel Lindau syndrome
223
CF of a phaechromocytoma?
- can be bilateral or unilateral
- episodic
- HTN - v high
- headaches
- palpitations
- anxiety
- sweating
224
Ix of a phaechromytoma - 1)
- 24 hr urine metanephrines NOT catecholamines
225
Other Ix for a phaechromocytoma?
- CT/ MRI
- Functional imaging modalities like MIBG scintigraphy or PET scans may be employed in cases of metastatic or extra-adrenal disease.
- genetic testing e.g. VHL
226
Mx of phaechromocytoma?
- Surgery definitive
- but medically stabilise with BB or alpha blocker like phenyoxybenzamine first - pre-op
227
most common cause of primary hyperaldosteronism?
- bilateral idiopathic adrenal hyperplasia causes most cases followed by adrenal adenomas
228
Top 2 causes of primary hyperaldosteronism?
1) bilateral adrenal hyperplasia
2) Conns = adrenal adenoma
229
CF of primary hyperalds?
- HTN
- hypokalaemia - e.g. muscle weakness
- metabolic alkalosis
230
When should Conns be suspected?
- hypertension w hypokal
- Tx resistant HTN
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First line Ix in primary hyperalds?
- first line: plasma A/R ratio
- should show high aldosterone levels alongside low renin levels (negative feedback due to sodium retention from aldosterone
232
Other Ix for PHA?
- High res CT abdo and adrenal vein sampling can be done to distinguish between unilateral and bilateral hyperplasia
233
Secondary hyperaldosteronism is caused by?
caused by excessive renin stimulating the release of excessive aldosterone.
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SHA: Excessive renin is released due to disproportionately lower blood pressure in the kidneys, usually due to:
- Renal artery stenosis
- Heart failure
- Liver cirrhosis and ascites
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Ix of Renal artery stenosis?
- Renal artery stenosis (atherosclerosis of renal artery) is confirmed w Doppler US and CT angiogram oe MRA
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ARR result interpretation?
- High aldosterone and low renin indicate primary hyperaldosteronism
- High aldosterone and high renin indicate secondary hyperaldosteronism
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Mx of primary HA?
- eplerenone and spironolactone - aldosterone antagonists
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who should we consider testing for hyperalds in?
- Consider testing for hyperaldosteronism in patients with hypertension, who are younger, fail to respond to treatment or have a low potassium.
- Be aware that potassium levels may be normal in hyperaldosteronism.
239
Complication of immune checkpoint inhibitors?
- Addisons is a complication of ICI
- ACTH excess (lack of negative feedback)
- T cells activated by ICIs may mistakenly recognize adrenal antigens as foreign and mount an immune response against them, leading to adrenal gland inflammation.
240
CFs of addisons?
- fatigue weakness and lethargy
- hypotension - dizziness, fainintg, lightheadedness
- Nausea, vomiting, abdo pain
- Hyponatreamia
- Hypoglycaemia - cortisol deficiency
241
confirmation of addisons through...
synthacten
242
hypophysitis is...
- inflammation of PG -> inadequate production of one or more of the hormones secreted by the pituitary gland.
243
most common cause of hypophysitis?
- compression of the pituitary gland by non-secretory pituitary macroadenoma (most common)
244
Pituitary causes of hypophysitis?
- pituitary apoplexy
- Sheehan's syndrome: postpartum pituitary necrosis secondary to a postpartum haemorrhage
- hypothalamic tumours e.g. craniopharyngioma
245
other causes of hypophysitis?
- trauma
- iatrogenic irradiation
- infiltrative e.g. hemochromatosis, sarcoidosis
246
Hypophysitis - low ACTH?
- tiredness
- postural hypotension
247
Hypophysitis - low FSH/LH?
- amenorrhoea
- infertility
- loss of libido
248
Hypophysitis - low TSH?
- feeling cold
- constipation
249
Hypophysitis - low GH?
- if occurs during childhood then short stature
250
Hypophysitis - low prolactin ->
- problems with lactation
251
Pituitary macroadenoma vs apoplexy?
- pituriary macroadenoma → bitemporal hemianopia
- pituitary apoplexy → sudden, severe headache
252
Mx of hypophysitis?
- replacement of deficient hormones
- Tx of underlying cause - e.g. surgery for removal of tumour
253
drugs causing hypopituitarism?
- high dose steroids
- Checkpoint Inhibitors
254
med induced adrenal insufficiency?
- Prolonged use of glucocorticoids or drugs that inhibit steroidogenesis (e.g., ketoconazole) can suppress the hypothalamic-pituitary-adrenal (HPA) axis, leading to adrenal atrophy and insufficiency.
255
what can lead to adrenal haemorrhage -> adrenal insufficiency?
- Trauma, anticoagulation, and sepsis can lead to adrenal haemorrhage, resulting in acute adrenal insufficiency.
256
Physiological causes of hyperprolactinaemia?
- stress
- pregnancy
- lactation
- exercise
- sexual intercourse
257
Drugs causing hyperprolactinaemia?
- AP
- AD - SSRIs, MAO inhib, antienetics like domperidone and metoclopramide
258
most common cause of pathological hyperprolactinomas?
prolactinomas
259
hyperprolactinomas - compression of pituitary stalk?
Compression of pituitary stalk due to meningiomas, craniphrayngiomas, GH secreting adenomas -> acromegaly
260
other causes of hyperprolactinomas?
- CKD, cirrhosis, PCOS, hypothyroidism
261
lab investigations of prolactinomas?
* Serum prolactin: to confirm the diagnosis of hyperprolactinaemia
* Pregnancy test: to exclude pregnancy, a common physiological cause of hyperprolactinaemia
* Thyroid function tests: to identify hypothyroidism
* Urea & electrolytes: to identify reduced renal function (chronic kidney disease)
* Pituitary function testing: to assess pituitary function and possible hypopituitarism
262
Ix of a prolactinomas?
- type of pituitary adenoma
- macroadeoma >1cm
- hormonal status: a secretory/functioning adenoma produces and excess of a particular hormone and a non-secretory/functioning adenoma does not produce a hormone to excess
263
Features of a prolactinoma - excess prolactin in women?
amenorrhoea
- infertility
- galactorrhoea
- osteoporosis
264
Features of a prolactinoma - excess prolactin in men?
- impotence
- loss of libido
- galactorrhoea
265
Symptoms seen in a macroadenoma?
- headache.
- visual disturbances (classically, a bitemporal hemianopia (lateral visual fields) or upper temporal quadrantanopia)
- symptoms and signs of hypopituitarism
266
diagnosis of a pituitary adenoma?
MRI
267
Medical management of a prolactinoma?
- in the majority of cases, symptomatic patients are treated medically with dopamine agonists (e.g. cabergoline, bromocriptine) which inhibit the release of prolactin from the pituitary gland
268
Surgical Mx of prolactinomas?
- surgery is performed for patients who cannot tolerate or fail to respond to medical therapy.
- A trans-sphenoidal approach is generally preferred unless there is a significant extra-pituitary extension
269
Follow up for prolactinomas
- Follow up every 6 -12 months
- measurement of prolactin levels
- visual fields
270
Signs of non-functioning tumours of PG - mass effects?
- headache
- bilateral heminaopia
- symptoms of hypopituitarism
271
2 initial tests in DI?
- 1) Water deprivation
- 2) desmopressin
272
Cranial DI vs nephrogenic DI?
- cranial DI: increase conc of urine after desmopressin
- Nephrogenic: no change following desmopressin
273
sIADH ?
- Increased release of ADH from PP
- increases water reabs from the urine, causing dilution of the blood -> hyponatreamia
274
DI vs siADH?
- DI: hypernatreamia
- siADH: hyponatraemia
275
Pathophys of sIADH?
- ADH produced in the hypothalamus and secreted the PP
- ADH stimulates water reabs in CDs diluting blood
- causes hyponatreamia
- extra water doesn't cause fluid overload so this is a euvolaemic hyponatreamia
276
Urine osmolarity vs sodium?
- high urine osmolarity
- high urine sodium
277
The symptoms of SIADH relate to low sodium (hyponatraemia). Depending on the sodium level and how rapidly it occurs, they may be asymptomatic or present with non-specific symptoms:
- Headache
- Fatigue
- Muscle aches and cramps
- Confusion
278
Severe hyponatraemia- >
seziures and reduced consciousness
279
causes of siADH?
- pre-op after surgery - transphenoidal surgery
- lung infection
- subarachnoid haemorrhage
- Meds - SSRI and carbamazepine
- small cell lung cancer
- HIV
280
pre-op after surgery?
transsphenoidal surgery
281
CFs of siADH?
- Euvolaemia
- Hyponatraemia
- Low serum osmolality
- High urine sodium
- High urine osmolality
282
Excluding other causes w siADH?
- synacthen test
- CKD
- HF or liver disease
283
Primary polydipsia?
- primary polydipsia involves excessive water consumption.
- Causes euvolaemic hyponatreamia but there is low urine sodium and low urine osmolality
284
Mx of siADH?
- Stop med and treat underlying infection
- Fluid restrict
- Vasopressin antagonists - tolvaptan
285
why must sodium be corrected slowly?
- It is essential to correct the sodium slowly to prevent osmotic demyelination. The sodium concentration should not change more than 10 mmol/L in 24 hours.
286
287
hyponatreamia - fluid must be?
Patients should be fluid restricted, to increase serum sodium and correct the hyponatremia
