Endo Flashcards
Addison’s Disease - Definition & Presentations
Primary Adrenal Insufficiency -> A disorder that affects the cortex of the adrenal glands, which means the synthesis and secretion of steroids is impaired
Most import steroids affected are: Cortisol, Aldosterone & DHEA
Presentations:
- Raised ACTH
- Decreased Cortisol ,etc..
- Fatigue
- Anorexia
- Weight Loss
- Hyperpigmentation
- Nausea
- Postural hypotension (due to fluid imbalance)
- Salt cravings
Addison’s Disease - Aetiology & Risk Factors
Most cases are Autoimmune related - usually autoantibodies to 21-hydroxylase
Often associated with other autoimmune diseases:
- Hashimoto’s
- Grave’s disease
- T1DM
Can also be caused by:
- Infectious diseases
- Metastatic diseases
- Haemorrhagic infarction of adrenal glands
- Surgical bilateral adrenalectomy
Risk Factors:
- Female sex
- Adrenocortical autoantibodies
- Adrenal Haemorrhage
- Autoimmune disease
- Coeliac disease
-FHx of Autoimmune diseases
Addison’s Disease - Epidemiology
Primary adrenal insufficiency is a rare condition with an overall prevalence of about 100 to 140 cases per million and an incidence of 4:1,000,000 per year in developed countries
In developed countries, autoimmunity is the main cause of primary adrenal insufficiency and, as women are at greater risk than men of acquiring an autoimmune disease, this cohort is predominantly women.
Addison’s Disease - Differentials
1) Adrenal suppression due to use of glucocorticoid/ drugs with glucocorticoid activity
-> Check history, no hyperpigmentation, lowered ACTH
2) Central (secondary or tertiary) adrenal insufficiency
-> Check history for brain lesions or surgeries (hypothalamus/pituitary)
-> CT scan
-> lowered ACTH
-> Lowered pituitary hormones
3) Haemochromatosis
-> Very different disease affecting iron absorption, but can present similarly.
-> Hyperpigmentation rarely involves mucosa
-> Test for iron levels & ACTH/cortisol levels
4) Hyperthyroidism
-> Elevated T3/4 & suppressed TSH
-> Tremor, tachycardia
-> Unexplained weight loss despite good appetite
5) Occult Malignancy (undetected)
-> Varies depending on Malignancy
6) Anorexia Nervosa
-> Fear of gaining weight, body dysmorphia, weight loss, amenorrhoea
->Psychological
Addison’s Disease - Investigations
1st Order Investigations:
- Morning Serum Cortisol -> Should be low
- Plasma ACTH -> Should be high
- Serum electrolytes -> low sodium and high potassium serum levels is typical
- U&C -> elevated blood urea and creatinine
- FBC -> anaemia, eosinophilia, relative lymphocytosis, and neutropenia
Consider:
- Plasma Renin activity
- ACTH stimulation test
- Adrenal antibodies
- Adrenal CT/MRI
Addison’s Disease - Management
1st Line:
- Intravenous hydrocortisone & supportive therapy -> for suspected but unconfirmed diagnosis to prevent adrenal crisis
-> Saline, 1L rapidly then 4-6L over 24 hours
-> Glucose to correct hypoglycaemia as needed
-> Find underlying cause and treat
->hydrocortisone sodium succinate: 100 mg intravenously/intramuscularly as a single dose, followed by 200 mg per 24 hours as a continuous infusion
Chronic treatment:
-> Oral glucocorticoid & mineralocorticoid replacement therapy
-> If Pregnant, must monitor every 6-8 weeks as there may be an increased need
-> Give Hydrocortisone/cortisone/prednisolone & fludrocortisone
-> Must be careful when ill
Addison’s Disease - Prognosis & Complications
Prognosis:
Patients should receive replacement therapy for life
Complications:
- some patients complain of persistent fatigue and decreased well-being
- Secondary Cushing’s Syndrome -> Over-replacement of glucocorticoids can lead to development of signs and symptoms of Cushing syndrome (weight gain and facial plethora) -> should lower Glucocorticoid dosage
- Osteopenia/Osteoporosis -> Associated with long-term excessive glucocorticoid replacement -> If no other cause can be found, decrease glucocorticoid
-Treatment-related hypertension -> Excessive mineralocorticoid replacement manifests with hypertension and hypokalaemia
- Adrenal Crisis if not managed/treated
-> Extreme lowered Cortisol
-> Life threatening
-> Cortisol is vital for regulating blood sugar, blood pressure, and electrolyte balance. Without sufficient cortisol, the body can go into a state of shock, leading to a rapid decline in vital functions
Acute pancreatitis - Definition & Presentations
A disorder of the exocrine pancreas, and is associated with acinar cell injury with local and systemic inflammatory responses
The severity of the disease varies:
- Most patients will have mild disease with minimal pancreatic oedema, and will recuperate fully within a few days
- A minority of patients will have severe disease, characterised by a persistent systemic inflammatory response and/or multi-organ failure, with or without pancreatic/peripancreatic necrosis
Presentations:
- upper abdominal pain
- nausea and vomiting
- signs of hypovolaemia
- signs of pleural effusion
- anorexia
Acute pancreatitis - Aetiology & Risk Factors
Gallstones and alcohol misuse
-> account for at least half of cases of acute pancreatitis
1/3 Idiopathic
Can be caused by: Trauma, drugs, Autoimmune conditions, hypercalcaemia, etc…
Risk Factors:
- Middle-aged Women/men
- Gallstones
- Alcohol
- Hypertriglyceridemia
- Use of Causative drugs
- Trauma
Acute pancreatitis - Differentials
1) Peptic ulcer disease
-> May improve with proton pump inhibitors, lifestyle modifications, and H pylori treatment
-> Normal or low lipase and amylase
2) Perforated viscus
-> Normal or slightly elevated lipase
-> Plain x-rays show sub-diaphragmatic air
3) Oesophageal spasm
-> A swallow study may demonstrate a contracted and abnormal-appearing oesophagus with increased pressures on oesophageal manometry
-> Dysphagia, odynophagia, weight loss, history of retrosternal pain
4) Intestinal obstruction
-> An abdomen/pelvic CT scan may be more diagnostic, and will show point of transition and potentially identify aetiology (such as volvulus, hernias, intussusception, masses)
-> Hernias, usually with incarcerated bowel, in the physical examination
5) Viral gastroenteritis
-> Important to obtain serum electrolytes and an FBC
-> Stool examination for microscopy, culture, osmolality, ova, parasites, Clostridium difficile toxin, and white blood cells may help in identifying the causative factor
Acute pancreatitis - Investigations
Suspect a diagnosis of acute pancreatitis in any person who presents with Acute sudden-onset upper or generalized abdominal pain, which may be associated with:
- Nausea and/or vomiting.
- A history or clinical features of gallstones, alcohol misuse, or other risk factors
-> Is usually a self-limiting viral infection but if fever is documented, bacterial and invasive organisms should be suspected
Acute pancreatitis - Management
Arrange emergency hospital admission if a person has suspected acute pancreatitis, for immediate specialist assessment and management.
-> DO NOT delay admission by arranging blood tests or imaging in primary care
In Hospital Acute:
- Resuscitation with intravenous fluids
- Supplemental oxygen
- Intravenous analgesia
-> Ibuprofen: 300-600 mg orally (immediate-release) every 6-8 hours when required, maximum 2400 mg/day - Antiemetic
-> Ondansetron: 4-8 mg orally/intravenously/intramuscularly every 12 hours - Intravenous antibiotics for treatment of infected pancreatic necrosis and/or associated cholangitis
-> Imipenem/Cilastatin: 500-1000 mg intravenously every 6 hours - Early nutritional support which may involve initial parenteral feeding if the person is unable to tolerate oral intake
If failure to improve in 5-7 days:
1) Contrast-enhanced computed tomography (CECT) -> to see why
2) Continue other support given + add intervention for what you find on CECT
i.e.
stronger intravenous antibiotics for infected pancreatic necrosis,
catheter drainage/necrosectomy if sterile pancreatic necrosis or symptomatic sterile pseudocyst,
Both if infected pseudocyst (abscess)
Acute pancreatitis - Prognosis & Complications
The majority of patients (around 80%) with acute pancreatitis have mild disease and will improve within 3 to 7 days of conservative management
The overall mortality rate is low (approximately 5%) but this rises to 25% to 30% in severe acute pancreatitis
May progress to recurrent acute pancreatitis or chronic pancreatitis, and the risk is higher among people who smoke or drink alcohol to excess, and in men
Complications:
- Acute renal failure
-> Seen in patients with severe acute pancreatitis
-> Seen in patients with severe acute pancreatitis
- Sepsis
