Block 32 Week 8 Flashcards
acute pancreatitis?
- acute inflammation of the pancreas
- uncontr release of activated pancreatic enzymes -> autodigestion
most common cause of acute panc?
1) Gallstones
2) alcohol
I GET SMASHED
gallstones -> panc?
- most common cause
- almost half of cases
- can obstruct the ampulla -> biliary reflux
alcohol -> acute panceatitis?
- increased production of digestive enzymes
- alcohol commonly causes chronic panc but also causes acute
ERCP?
-> acute panc
endocrine function of pancreas?
- islets of langerhans
- insulin and glucagon
exocrine function of panc?
- pancreatic ductal cells
- produce pancreatic juice
- trypsin imp in pancreatitus
pain in acute panc?
- sudden onset epigastric pain
- vomiting
- worse on movement
- radiation to back
why may patients have reduced urinary output in panc?
- 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
Sx of acute panc?
- Abdominal pain (may radiate to the back)
- Nausea
- Vomiting
- Anorexia
- Diarrhoea
Signs of acute panc?
- Abdominal tenderness
- Abdominal distention
- Tachycardia
- Tachypnea
- Pyrexia
Acute panc - 2 signs?
Cullens sign and grey turners
Cullens sign =
peri-umbilical bruising
grey turner sign?
flank bruising
diagnostic test of acute panc?
amylase 3x the reference range
how long does amylase stay elevated?
- 3 days
- patients who present late may have a missed peak
amylase in acute on chronic panc?
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.
mild elevation of amylase?
- parotitis
- bowel obstruction
- intestinal inflammation
- trauma
- malignancy
- ruptured ectopic pregnancy
Lipase vs amylase?
- lipase is more specific for panc
- has a longer half life so levels remain elevated for longer
lipase levels suggesting acute panc?
3x above reference range
bedside Ix for acute panc?
- Observations
- ECG
- Blood sugar
- Pregnancy test
Bloods for panc?
- amylase/ lipase
- U&Es
- LFTs - assessing for cholangitis
- LDH
- glucose
- lipids
US in acute panc?
used to demonstrate gallstones or a dilated common bile duct. The pancreas may be visualised.
CT in acute panc?
used to confirm diagnosis when uncertainty remains and to exclude complications of disease.
MRCP in acute panc?
most commonly indicated in suspected gallstone pancreatitis to help evaluate for CBD stones.
scoring for acute panc?
glasgow
glasgow score indicating severe panc?
> 3
Tx of acute panc?
- supportive
- IV fluids
- Analgesia
- Nutritional support
nutrition in acute panc?
in mild cases low fat diet reintro
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.
when should ab be used?
- NOT for acute panc
- should be used for suspected cholangitis
ERCP?
- Gallstone panc
- stone extraction
pancreatic necrosis?
- continued inflammation -> local thrombosis, haemorrhage and necorsis in the panc
- high infection risk
- major cause of mortality
Ix for pancreatic necrosis?
- CT guided fine needle aspiration and culture
panc pseudocyst?
- present 4+ weeks after an episode
- psudo means epithelial lining around the cyst rather than granulation tissue
vascular complications of acute panc?
- pseudoaneurysm
- venous thrombosis
pseudoaneurysm?
- rare but life threatning haemorrhages
- often seen in splenic and hepatic arteries
- normally occur in association w pancreatic pseudocysts
venous thrombosis?
- venous thrombosis may affect the portal, splenic and superior mesenteric veins
- requires AC
Severe acute pancreatitis can lead to ->
- Acute respiratory distress syndrome
- Renal failure
- Shock - disrtibutive
mortality in acute panc?
- 1% in mild panc
- sterile pancreatic necrosis: 10%
- infected panc necrosis: 25% mortality
Chronic pancreatitis refers to
chronic, irreversible, inflammation and/or fibrosis of the pancreas.
leading cause of chronic panc?
alcohol
endocrine dysfunction in chronic panc?
Endocrine dysfunction: damage to the islet cells result in lack of insulin and development of diabetes mellitus
exocrine dysfunction in chronic panc?
Exocrine dysfunction: damage to the acinar cells results in lack of pancreatic enzymes and malabsorption
Classification of the causes of panc?
TIGAR-O
Tigar-O?
T (toxic/metabolic): alcohol, smoking, high triglycerides, hypercalcaemia, chronic kidney disease
tIgar-O?
- idiopathic
- may be late onset, early onset or tropical
tiGar-O?
- genetics
- mutation in PRSS1
autoimmune panc?
- type 1
- type 2
Type 1 autoimmune panc?
- IgG4 disease
Type 2 autoimmune panc?
limited to the pancreas and associated with inflammatory bowel disease
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
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
autosomal dominant hereditary panc?
- PRSS1 mutation
- encodes cationic trypsinogen
autosomal recessive hereditary panc?
- mutation in CTFR gene
- spink 1 gene
most common feature of chronic panc?
abd pain
pain in chronic pain?
- epigastric discomfort
- worse post-prandially and on lying down
pain in chronic panc may be assoc w ?
- nausea
- vomiting
- anorexia
CP - exocrine insufficiency?
- destruction of acinar cells -> loss of digestive enzymes -> malabs
- inability to digest fatty foods due to lack of lipase
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
loss of endocrine cells in CP?
- Type 3c DM
- Polyuria, polydispsia, weight loss
assessment of chronic panc?
- CT or MRI with MRCP
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).
Fecal elastase?
- indirect marker of panc function
- used to assess for panc exocrine insufficiency
- low levels suggest PEI
Bloods in CP?
- FBC, U&Es, LFTs
- lipid profile
- bone profile
- mag
- hbalc
general management of chronic panc?
- nutritional assessment
- alcohol cessation
- smoking cessation
- vitamin replacement e.g. vitamin D
Pain relief in chronic panc?
- basic first: paracetamol and NSAIDs
- then weak opiods: tramadol, codeine
PEI management?
- pancreatic enzyme replacement therapy
- abs can be improved using a PPI
Endoscopic management for chronic panc when:
- Pancreatic pseudocysts
- Pancreatic stones
- Main pancreatic duct strictures
- Other complications (e.g. biliary strictures,
duodenal obstruction)
complications of chronic panc?
- PEI
- DM
- osteoporosis
- panc cancer
- duodenal and biliary obst
Hb ab interpretation?
HBsAg = ongoing infection, either acute or chronic if present > 6 months
anti-HBc = caught, i.e. negative if immunized
Transmission of hep A?
- faecal-oral
hep A disease coruse?
- self limiting
- doesn’t cause chronic disease
features of hep A?
- flu-like prodrome
- abdominal pain: typically right upper quadrant
- tender hepatomegaly
- jaundice
- deranged liver function tests
immunisation for hep?
- A
- B
hep B is a
double standed DNA hepadanvirus
how is hep B spread?
- exposure to infected blood or body fluids
- mother to child
incubation period for hep B?
6-20 weeks
features of hep B?
- fever
- jaundice
- elevated LFTs
features of chronic hep B on LM?
ground glass hepatocytes
complications of hep B
- HCC
- glomerulonephritis
- fulm liver failure
hep E spread?
- faecal oral
- Can be transmitted by seafood
incubation period of hep E?
3-8 WEEKS
Where is hep E common?
- central and south asia
- mexico
- north and west africa
hep E is especially problematic in?
- pregnancy - causes sig mortality
hep E does not cause ?
does not cause chronic disease or an increased risk of hepatocellular cancer
hep C affects?
- IV drug users
- patients who receive a blood transfusion
incubation period of hep C?
6-9 weeks
transmission of HepC?
- Needle stick injury
- mother to child
- sexual intercourse
what is not contra-indicated in hep C?
breastfeeding
there is no vaccine for ?
hep C
Comps of chronic hep C?
- Sjogren’s syndrome
- cirrhosis
- HCC
- glomerulonephritis
hep D?
- single stranded RNA virus
- transmitted parenterally (blood and body fluids)
how does hep D cause infection?
- requires hep B surface antigen to repllicate
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.
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.
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.
Ascending cholangitis is?
- infection of the biliary ducts
- caused by obstruction
how does ascending cholangitis present?
Charcots triad: fever, jaundice, RUQ pain
Reynol’d pentad?
- Ascending cholangitis
- fever, jaundice, RUQ pain, septic shock and mental confusion
common causes of asc cholamgitis?
choledocholithiasis (gallstones) and strictures of the biliary tree.
Reynold’s pentad indicated?
inc risk of septic shock -> medical emergency
LFTs with Ascending cholangitis?
hyperbilirubinaemia and elevated serum alkaline phosphatase
imaging for Ascending cholangitis?
- ERCP: when history of biliary disease
- transabd US: CBD dilatation
Mx of ascending cholangitis?
- pieracillin/ tazobactam
- IV fluids
- analgesia
- sepsis 5
definitive management of ascendinh cholngitis?
- biliary decompression
- ERCP or surgery
biliary colic pain?
- RUQ pain
- intermittent
- usually begins abruptly and subsides gradually
- attacks often occur after eating
Biliary colic - mneumonic?
- female
- forties
- fat
- fair
Acute cholesystitis pain?
- similar to biliary colic but more severe and persistent
- pain may radiate to back or right shoulder
acute cholesytitis sign?
- pyrexial
- murphy’s sign positive: arrest of inspiration on palpation of the RUQ
Gallstone ileus?
- SBO
- secondary to impacted gallstone
features of gallstone ileus?
Abdominal pain, distension and vomiting
Features of cholangiocarcinoma?
- persistent biliary colic symptoms
- anorexia
- jaundice
- weight loss
Signs of cholangiocarcinoma?
- Courvoiser’s sign
- sister mary joseph nodes
- virchow node
Courvoisier sign?
palpable mass in the right upper quadrant
Sister mary joseph nodes?
periumbilical lymphadenopathy
virchow node?
left supraclavicular adenopathy
acute panc pain is usually due to?
alcohol or gallstones
features of acute panc pain?
- Severe epigastric pain
- Vomiting is common
- Examination may reveal tenderness, ileus and low-grade fever
pancreatic cancer features?
- painless jaundice
- anorexia
- weight loss
differentiating pain
- Biliary colic –> pain
- Acute cholecystitis –> pain + fever
- Ascending cholangitis –> pain + fever + jaundice
Mirrizi syndrome?
In Mirizzi syndrome the stone may compress the bile duct directly- one of the rare times that cholecystitis may present with jaundice
infection in cholangitis is due to?
E coli
Panc cancer?
Typically painless jaundice with palpable gallbladder (Courvoisier’s Law)
cholangiocarcinoma is linked to
PSC
RF for gallstones?
- Fat
- Female
- Fertile - pregnancy
- Forty
Other RF for gallstones?
- diabetes
- chrons
- rapid weight loss
- drugs - fibrates, oral contraceptive
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
distinguishing biliary colic from other gallstone related conditions?
in biliary colic there is no fever and liver function tests/inflammatory markers are normal
choledocholithiasis=
gallstones in common bile duct
cholelithiasis =
Cholelithiasis (gallstones) refers to the development of a solid deposit or ‘stone’ within the gallbladder.
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.
RF for gallstones?
- age
- female
- obesity
- rapid weight loss/ prolonged fasting
- diabetes
- crohns
medications linked to gallstones?
oestrogen replacement therapy, ceftriaxone, octreotide
CF of gallstones?
- intermittent RUQ/ epigastric pain
- nausea and vomiting
Ix for gallstones?
- USS - can also assess for CBD dilation
- LFTs
symptomatic management of gallstones?
- analgesia - paracetamol and NSAIDs
- diet - low fat
surgical management of gallstones?
- elective cholecystectomy
cholethiasis refers to?
Cholelithiasis (gallstones) refers to the development of a solid deposit or ‘stone’ within the gallbladder.
Choledocholithiasis =
gallstones within the biliary tree.
biliary colic =
refers to a self-limiting pain in the RUQ/epigastrum associated with gallstones.
acute cholecystitis =
refers to the acute inflammation of the gallbladder, most commonly caused by gallstones.
acute cholangitis =
refers to the acute inflammation of the gallbladder, most commonly caused by gallstones.
cholesterol stones?
- most common type
- occur due to crystalisation of cholesterol in bile due to supersaturation of cholesterol
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
brown pigment stones?
- mix of calcium bilirubinate and a calcium salts of fatty acids
- mostly occur in association with infection
comparison of abd pain?
biliary colid observations?
- normal
- BTs normal
acute cholesystitis symptoms?
RUQ pain, fevers, malaise
observations of acute cholesytitis?
- fever
- haemodynamic instability
examination in acute cholesystitis?
- tenderness
- localised guarding may be present
USS of acute cholesystitis?
- gallstones
- inflamed, thickened GB
- pericholesytitic fluid
acute cholangitis obs?
fever and haemodynamic instability
acute cholangitis features?
- jaundice
- tenderness
acute cholangitis findings on US?
CBD stone, duct dilatation
acute panc summary?
- epi pain radiating to back
- fever and tachy
- epigastric tenderness
- raised amylase
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.
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
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.
diabulimia?
- diabulimia involves the deliberate manipulation of insulin doses to control weight -> poor glycaemic control and ketosis
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
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
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
Interventions to reduce risk and manage CVD - T1D?
- Stop smoking
- BB for those who have had a stroke or MI
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.
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.
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.
appetite control centre is in the?
- in the hypothalamus
- arcuate nucleus -> appetite controle
excitatory vs inhibitory NTs?
- Excitatory neurons release NPY -> hunger
- Inhibitory neurons release -> POMC
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
PPY?
from the ileum in response to feeding. Causes appetite suppression
Leptin?
- leptin is produced by fat cells
- stimulates inhibitory neurones and inhibits excitatory neurons in the arcuate nucleus -> appetite suppression
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.
How does the stomach signal to the brainstem?
vagus nerve
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
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
LT metabolism regulation?
- High fat -> stop feeding and spend energy
- Low fat -> feed more, preserve more energy
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
Obesity results from?
- results from disregulation of this system
- assoc w chronic low leptin - makes the body think its starved which leads to obesity
Lifestyle in obesity development?
- high fat diet -> saturated fats -> inflammation -> leptin resistance -> starvation response
- Leptin deficiency or mutations leading to leptin resistance
Roles of insulin?
- Insulin -> GLUT4 insertion -> glucose enters cell
- Causes glycogen production, inhibits glucogonegenesis
Roles of glucagon?
- Glucagon - released when all the glucose
- inactivates glycogen synthesis
- inc glucogenolysis
- Adrenaline acts the same as glucagon but faster
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
-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
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
Waist circumference indicating obesity?
Men: ≥ 102 cm (40 inches)
Women: ≥ 88 cm (35 inches)
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
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
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.
when is bariatric surgery indicated in obesity?
BMI > 40
Least restrictive bariatric surgery?
LABG
LABG
- least restrictive
- first line
- less weight loss but less comps
What does a sleeve gastrectomy do?
reduces size of stomach
What does the duodenum abs?
= Metal ions + Folate (first)
Jejenum vs ileum abs?
- Jejunum = all vitamins except
- Ileum = B12
What does the LI abs?
Na, K, water
Initial Ix of Pituitary disease?
- ACTH
- FSH/ LH
- TSH
- GH
- prolactin
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
RF for Thyroid eye disease?
- most imp: smoking
- radiodine treatment - predinoslone can reduce risk
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
Mx of thyroid eye disease?
- smoking cessation
topical lubricants may be needed to help prevent corneal inflammation caused by exposure - steroids
- radiotherapy
- surgery
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
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.
Roles of meds in causing thyrotoxicosis?
amiodarone and immune checkpoint inhibitors in causing thyroid hormone excess
Subclinical hyperthyroidism TFTs?
- normal T3 and T4 levels
- TSH is low (suppressed)
Causes of subclin hyperthyroidism?
MNG paticularly in elderly females
Problems in subclinical hyperthyroidism?
- AF
- osteoporosis
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
Subclinical hypothyroidism TFTs?
TSH raised T3 and T4 normal
Significance of subclin hypothyrodisim?
- risk of progressing to overt hypothyroidism - higher in men
- risk increased by presence of thyroid autoantibodies
Mx of subclin hypo?
- TSH >10 -> levothyroxine
What is an adrenal incentaloma?
- Incidentaloma - mass found upon imaging
- was not carried out for sus of adrenal disease
Signs and symptoms of adrenal incidentaloma?
- usually no typical findings
- mild autonomous cortisol excess
sig of an adrenal incidenataloma?
- Have an increased incidence of metabolic disease like T2DM, HTN, osteoporosis, dyslipidemia
Ix for an adrenal incidentaloma?
- CT for diagnostic uncertainty on whether it’s a cancer
- Urine metanephrines
- > 4cm mass requires urgent assessment for malignancy
Other Ix of adrenal incidentaloma?
- Glucocorticoids - Dexamethasone suppression test
- Urine and plasma metanephrines
Mx of an adrenal incidentaloma?
- Benign and no hormone excess -> no follow up
- Clinically overt cortisol excess or aldosterone or catecholamines -> surgery?
site of origin for a phaechromocytoma?
- chromaffin cells of the adrenal medulla -> catecholamine hypersecretion
- may also develop at extra-adrenal sites -> paraganlionomas
Triad for phaechromocytoma?
episodic headache, diaphoresis, and tachycardia
Diagnosis of phaechrocytoma?
- Plasma or urinary fractioned metanephrines
- Followed by CT/ MRI for localisation
associations
Pathophys of Phaechromoytoma?
- MEN11 association
- Von Hippel Lindau syndrome
CF of a phaechromocytoma?
- can be bilateral or unilateral
- episodic
- HTN - v high
- headaches
- palpitations
- anxiety
- sweating
Ix of a phaechromytoma - 1)
- 24 hr urine metanephrines NOT catecholamines
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
Mx of phaechromocytoma?
- Surgery definitive
- but medically stabilise with BB or alpha blocker like phenyoxybenzamine first - pre-op
most common cause of primary hyperaldosteronism?
- bilateral idiopathic adrenal hyperplasia causes most cases followed by adrenal adenomas
Top 2 causes of primary hyperaldosteronism?
1) bilateral adrenal hyperplasia
2) Conns = adrenal adenoma
CF of primary hyperalds?
- HTN
- hypokalaemia - e.g. muscle weakness
- metabolic alkalosis
When should Conns be suspected?
- hypertension w hypokal
- Tx resistant HTN
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
Other Ix for PHA?
- High res CT abdo and adrenal vein sampling can be done to distinguish between unilateral and bilateral hyperplasia
Secondary hyperaldosteronism is caused by?
caused by excessive renin stimulating the release of excessive aldosterone.
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
Ix of Renal artery stenosis?
- Renal artery stenosis (atherosclerosis of renal artery) is confirmed w Doppler US and CT angiogram oe MRA
ARR result interpretation?
- High aldosterone and low renin indicate primary hyperaldosteronism
- High aldosterone and high renin indicate secondary hyperaldosteronism
Mx of primary HA?
- eplerenone and spironolactone - aldosterone antagonists
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.
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.
CFs of addisons?
- fatigue weakness and lethargy
- hypotension - dizziness, fainintg, lightheadedness
- Nausea, vomiting, abdo pain
- Hyponatreamia
- Hypoglycaemia - cortisol deficiency
confirmation of addisons through…
synthacten
hypophysitis is…
- inflammation of PG -> inadequate production of one or more of the hormones secreted by the pituitary gland.
most common cause of hypophysitis?
- compression of the pituitary gland by non-secretory pituitary macroadenoma (most common)
Pituitary causes of hypophysitis?
- pituitary apoplexy
- Sheehan’s syndrome: postpartum pituitary necrosis secondary to a postpartum haemorrhage
- hypothalamic tumours e.g. craniopharyngioma
other causes of hypophysitis?
- trauma
- iatrogenic irradiation
- infiltrative e.g. hemochromatosis, sarcoidosis
Hypophysitis - low ACTH?
- tiredness
- postural hypotension
Hypophysitis - low FSH/LH?
- amenorrhoea
- infertility
- loss of libido
Hypophysitis - low TSH?
- feeling cold
- constipation
Hypophysitis - low GH?
- if occurs during childhood then short stature
Hypophysitis - low prolactin ->
- problems with lactation
Pituitary macroadenoma vs apoplexy?
- pituriary macroadenoma → bitemporal hemianopia
- pituitary apoplexy → sudden, severe headache
Mx of hypophysitis?
- replacement of deficient hormones
- Tx of underlying cause - e.g. surgery for removal of tumour
drugs causing hypopituitarism?
- high dose steroids
- Checkpoint Inhibitors
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.
what can lead to adrenal haemorrhage -> adrenal insufficiency?
- Trauma, anticoagulation, and sepsis can lead to adrenal haemorrhage, resulting in acute adrenal insufficiency.
Physiological causes of hyperprolactinaemia?
- stress
- pregnancy
- lactation
- exercise
- sexual intercourse
Drugs causing hyperprolactinaemia?
- AP
- AD - SSRIs, MAO inhib, antienetics like domperidone and metoclopramide
most common cause of pathological hyperprolactinomas?
prolactinomas
hyperprolactinomas - compression of pituitary stalk?
Compression of pituitary stalk due to meningiomas, craniphrayngiomas, GH secreting adenomas -> acromegaly
other causes of hyperprolactinomas?
- CKD, cirrhosis, PCOS, hypothyroidism
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
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
Features of a prolactinoma - excess prolactin in women?
amenorrhoea
- infertility
- galactorrhoea
- osteoporosis
Features of a prolactinoma - excess prolactin in men?
- impotence
- loss of libido
- galactorrhoea
Symptoms seen in a macroadenoma?
- headache.
- visual disturbances (classically, a bitemporal hemianopia (lateral visual fields) or upper temporal quadrantanopia)
- symptoms and signs of hypopituitarism
diagnosis of a pituitary adenoma?
MRI
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
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
Follow up for prolactinomas
- Follow up every 6 -12 months
- measurement of prolactin levels
- visual fields
Signs of non-functioning tumours of PG - mass effects?
- headache
- bilateral heminaopia
- symptoms of hypopituitarism
2 initial tests in DI?
- 1) Water deprivation
- 2) desmopressin
Cranial DI vs nephrogenic DI?
- cranial DI: increase conc of urine after desmopressin
- Nephrogenic: no change following desmopressin
sIADH ?
- Increased release of ADH from PP
- increases water reabs from the urine, causing dilution of the blood -> hyponatreamia
DI vs siADH?
- DI: hypernatreamia
- siADH: hyponatraemia
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
Urine osmolarity vs sodium?
- high urine osmolarity
- high urine sodium
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
Severe hyponatraemia- >
seziures and reduced consciousness
causes of siADH?
- pre-op after surgery - transphenoidal surgery
- lung infection
- subarachnoid haemorrhage
- Meds - SSRI and carbamazepine
- small cell lung cancer
- HIV
pre-op after surgery?
transsphenoidal surgery
CFs of siADH?
- Euvolaemia
- Hyponatraemia
- Low serum osmolality
- High urine sodium
- High urine osmolality
Excluding other causes w siADH?
- synacthen test
- CKD
- HF or liver disease
Primary polydipsia?
- primary polydipsia involves excessive water consumption.
- Causes euvolaemic hyponatreamia but there is low urine sodium and low urine osmolality
Mx of siADH?
- Stop med and treat underlying infection
- Fluid restrict
- Vasopressin antagonists - tolvaptan
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.
hyponatreamia - fluid must be?
Patients should be fluid restricted, to increase serum sodium and correct the hyponatremia
