Medicine B Flashcards
How should pyrexia in the returning traveller be investigated?
When assessing a fever in the returning traveller: T – Time of onset R – Room and board A – activities V – Vaccination E – exposure L – location
Pyrexia of Unknown Origin has multiple aetiologies including infective, inflammatory, autoimmune, neoplastic and miscellaneous. All patients with a PUO should have a HIV test and non-infective causes should be considered early on. Do not give empirical antibiotics or steroid trials and consider PET CT scanning.
What are the precipitating factors for DKA?
Precipitating factors include infections/sepsis, cardiovascular disease (Stroke or MI), discontinuation of insulin, inadequate insulin, new diagnosis of diabetes and medication induced such as when SGLT2 inhibitors are used.
What is the pathophysiology of DKA?
The pathophysiology is that the body has secreted no insulin at all so there is a dramatically reduced glucose uptake peripherally. Glucagon is secreted as the cells have no glucose. This causes uninhibited gluconeogenesis and glycogenolysis which increases the hyperglycaemic state. When there is too much glucose in the blood it is excreted by the kidneys which is known as glycosuria. Osmotic diuresis brings water with the glycosuria which causes severe dehydration.
Lipolysis also occurs in response to glucagon release and lack of glucose in target cells. Beta oxidation is the metabolic action which produces acetyl co-A and energy for cells. Acetyl coA goes into ketogenesis and produces ketone bodies which dissociate in the blood and cause metabolic acidosis.
What are the symptoms of DKA?
Polydipsia (extreme thirst), polyuria, weakness, weight loss, abdominal pain, nausea and vomiting, confusion and coma. Signs include acetone breath, kussmaul respiration (laboured deep breathing seen in metabolic acidosis), dry mucous membranes, dehydration, hypotension and tachycardia
How should DKA be investigated and treated?
Investigations include capillary blood glucose meter, ketone meter, urine dipstick and venous gas. Other investigations include FBC, U&E, CRP, ECG, CXR, urinalysis and blood cultures.
On presentation the management includes an ABCDE approach, IV insulin, IV fluids with potassium, anticoagulation, treating underlying causes such as infection, monitor fluid balances, repeat CBG, ketones, U&Es and venous HCO3. Escalate to critical care if severe.
What is a hyperosmolar hyperglycaemic state?
Hyperosmolar Hyperglycaemic State is defined as a serious complication of diabetes mellitus characterised by marked hyperglycaemia without ketonaemia or acidosis and hypervolaemia or hyperosmolarity. This usually occurs in T2DM and has a 15-20% mortality rate but occurs in less than 1% of T2DM patients.
What is the pathophysiology of HHS?
Precipitating factors include infection/sepsis, acute illnesses (MI, stroke, surgery or trauma), dehydration and a new diagnosis of T2DM. The pathophysiology is due to relative insulin deficiency. There is not enough insulin to allow glucose uptake in the peripheries but there is enough to prevent lipolysis and ketogenesis. Counter regulatory hormones are activated which causes gluconeogenesis and glycolysis and hence hyperglycaemia ensues. The patient will also have glycosuria with osmotic diuresis and dehydration with increased thirst. Hyperosmolarity leads to renal failure.
What are the clinical features of HHS?
Clinical features include fatigue, weight loss, polyuria, polydipsia, dehydration, tachycardia, hypotension, shock and an altered mental status such as confusion or coma. It is diagnosed on the bases of hypovolemia, marked hyperglycaemia (above 30mmol/l) without ketonaemia or acidosis and with hyperosmolarity (>320).
How should HHS be investigated and treated?
Investigations include CBG, venous gas, ketone meter, FBC, U&E, CRP, ECG, CXR, urinalysis, blood cultures and input/output chart. Management is with ABCDE assessment, intravenous insulin, potassium in IV fluids, anticoagulation, treating underlying causes, repeating CBG, osmolarity and UE and involving critical care if needed.
Describe the pathophysiology of hypoglycaemia
This is defined as a reduction in plasma glucose levels which is low enough to result in signs and symptoms. Generally, this is levels less than 4mmol/L. It is always important to assess why this has happened.
Hypoglycaemia can be caused by excessive insulin dosing, sulphonylureas, exercize, insufficient food intake, missed meals, impaired awareness, alcohol inhibition of glycogenolysis and reduced renal clearance of insulin which occurs in elderly patients. Non-diabetic causes include post prandial hypoglycaemia, post gastrectomy, critical illness (hepatic, renal or cardiac failure and sepsis), prolonged fasting, malnutrition, hormone deficiencies and islet cell tumours.
What are the symptoms of hypoglycaemia?
Symptoms of hypoglycaemia include autonomic symptoms (<3.2 mmol/L) of sweating, nausea, palpitations, hunger, tremors and anxiety. At less than 2.5 mmol/L there can be cognitive dysfunction, visual changes, incoordination, confusion, aggression, seizures and coma.
What is Whipple’s Triad?
Signs and symptoms consistent with the diagnosis of hypoglycaemia, low plasma glucose and resolution of the symptoms once glucose is administered
How is hypoglycaemia classified?
- Mild: Plasma glucose between 3-3.9 mmol/L
- Moderate: Plasma glucose <3mmol activating a neuroglycopenic response
- Severe: Having low blood glucose affecting the mental or physical state and thus requiring 3rd party assistance
How should hypoglycaemia be managed?
Management is dependent on the GCS score as this determines how much glucose they need. Glucose levels should be rechecked 15-20 mins later.
What is Charcot foot?
Charcot Foot presents as a red, warm, painless swollen foot. It is often mistaken for cellulitis and osteomyelitis. Progressive pathological fractures and joint dislocation causes the Charcot formation and management is with emergency bed rest and total contact casting or removable walker.
The bony changes cause the shape of the foot to change to a “Rocker-Bottom” foot where the arch has collapsed, the foot is broadened, and the plantar aspect has a prominent midfoot. Recurrent ulceration is very common.
What are the causes and symptoms of hypothyroidism?
Causes of hypothyroidism include autoimmune conditions (Hashimoto’s), radioactive iodine, surgery, and drugs such as lithium and sulfonamides.
Symptoms include weight gain, lethargy, depression, hair loss, bradycardia, diastolic hypertension, constipation, menstrual disorders, cognitive impairment, voice changes, dry skin and goitre.
What are the causes and symptoms of hyperthyroidism?
Causes of hyperthyroidism include Graves (autoimmune), thyroiditis and thyroid nodules. The excess thyroid hormone causes increased metabolic rate and hence signs include anxiety, tremor, proximal muscle weakness, goitre, heat intolerance, exopthalmous, weight loss, hair loss, hypertension, widened pulse pressure, palpitations, tachycardia, AF and amenorrhoea or oligomenorrhoea.
How is hypothyroidism treated?
Levothyroxine
How is hyperthyroidism treated?
Hyperthyroidism is treated with anti-thyroid drugs such as Carbimazole and propylthoouracil. Symptomatic relief is provided with beta blockers. Permanent treatment is with radioiodine therapy or surgery.
What is coeliac disease?
Coeliac disease is a small bowel enteropathy in response to an immune mediated attack after gluten exposure. Symptoms include abdominal pain, lethargy, diarrhoea, bloating and weight loss.
What are the risk factors for coeliac disease?
Downs and Turner’s syndrome increases the risk of coeliac and Type 1 diabetes also increases the risk.
What are the extra-intestinal manifestations of coeliac disease?
Extra-intestinal manifestations include dermatitis herpetiformis which occurs in 15% of coeliac patients. This is treated with dapsone and topical steroids. Neuropathy and osteoporosis may also occur.
How is coeliac diagnosed?
Diagnosis is based on serology. Anti-IgA transglutaminase or endomysial antibodies are very accurate for diagnosis. Panel testing is not useful. Patients have to be eating gluten for 6 weeks prior to a TTG test. Biopsy of the duodenum can see scalloping and can be confirmed on histology. Diagnosis requires positive blood test and positive biopsy.
The histology is proven based on the March classification. Type 0 is normal, 1-2 is supportive but not diagnostic and 3 is suggestive of disease. HLA DQ5 and 8 genes are also required for coeliac disease (it is a genetic disease) and can be tested for in patients who refuse OGD.
Investigations include blood tests: Calcium, Vitamin D, TSH, HbA1c, FBC and LFTs. Also perform a DEXA scan if there are concerns about osteoporosis. Patients are also prone to pneumococcal infections and so may need vaccinations.
How is hyponatraemia subdivided?
Mild (130-134mmol/L)
Moderate (125-129mmol/L)
Severe (<125mmol/L).
What are the causes and symptoms of hyponatraemia?
Causes include medication, reduced blood volume, SIADH, renal salt wasting, Liver heart or renal failure, primary polydipsia or pseudohyponatraemia. Symptoms include nausea, vomiting, confusion, reduced GCS, headache and seizures.
How should hyponatraemia be investigated?
Always assess severity of symptoms, fluid status, signs of hypoaldosteronism (check cortisol), thyroid dysfunction and urine output. Always order a urine and serum osmolarity, urine U+Es, cortisol, TFTs and blood glucose. Pseudohyponatraemia can be caused by blood glucose and blood lipids.
How should hyponatraemia be treated?
Management is with correction which can be calculated by:
0.6 (total body water in non-elderly man) x weight (kg) x 0.5 (desired correction rate mmol/H)
Replacement is with sodium solution or saline.
How should hepatitis be investigated?
To investigate for Hepatitis, do bloods (FBC, U&Es, LFTs and clotting), HCV antibody screen and HIV, liver screen for autoantibodies, immunoglobulins and ferritin, USS and Fibroscan.
HbsAg: Indicates hepatitis B infection
Anti-HBc: Indicates current or past hepatitis B infection
Anti-HBc IgM: Usually indicates acute infection or reactivation
HBeAg: Indicator of a high level of HBV
Anti-HBs: Immunity either from recovery from Hep B infection or the vaccination.
How should hepatitis be treated?
Treatment is to prevent progression to cirrhosis, HCC and death. It will also reduce the risk of vertical transmission and risk of reactivation. HBV DNA should be reduced to undetectable levels. Treatment is dependent on the patient’s HBV DNA level, ALT and disease severity. Patients should also be treated if they have cirrhosis, or detectable HBV DNA.
Treatment is with Peg Interferon as a subcutaneous injection. Oral treatment is with tenofovir and entecavir. Prevention is with the vaccine which requires three doses. This is offered in the UK to IVDU/sex workers and occupational patients.
Hepatitis D should be suspected in patients with hepatitis B, especially if it is severe and persistent. Co-infected patients have more progressive disease. Hepatitis C is transmitted horizontally and can be asymptomatic. It can cause chronic infection which is a risk factor for cirrhosis and cancer. There is no vaccination available for Hepatitis C. Treatment is with DAA such as Harvoni, Epclusa and Maviret. Treatment is dependent on the patient’s genotype, evidence of compensated or decompensated cirrhosis and side effects.
What are the risk factors for NAFLD?
Risk factors for fatty liver disease are: Alcohol, drugs (Tamoxifen, amiodarone, methotrexate, corticosteroids and industrial solvents), metabolic syndrome, inherited conditions (Abetalipoproteinaemia, lipodystrophy and Wilson’s disease) and nutritional syndromes (rapid weight loss and JI bypass)
Fatty liver as a consequence of metabolic syndrome is more common in patients with obesity, raised triglycerides, insulin resistance, low HDL cholesterol and hypertension. Lean patients with NAFLD are of great concern.
How does NAFLD present?
Most patients are asymptomatic and are referred for abnormal LFTs. Symptomatic patients experience fatigue, RUQ discomfort, hepatomegaly and stigmata of chronic liver disease.
LFTs in NAFLD mainly present with elevated transaminases through raised ALP and GGT. The AST/ALT ratio is important as >0.8 suggests advanced cirrhosis. Ferretin may be elevated in half of patients and lipid profile or HbA1c is often elevated. These tests should be done to determine the risk of fibrosis.
Imaging is with USS of the liver to assess steatosis and complications of cirrhosis. MR spectroscopy is not easily available. The NAFLD or BARD score can be used to assess risks for a patient with NAFLD.
How should NAFLD be treated?
The main treatment is weight loss. Metabolic syndrome can also be targeted with statins or better management of any pre-existing diabetes. There is no liver directed pharmacology available. Finally, managing the complications of cirrhosis is the final step.
What is pseudohyponatraemia?
Pseudohyponatremia means spuriously reduced sodium results. Below 135 due to the presence of increased plasma lipid and/or increased plasma protein concentrations. The most common cause is hypercholesterolemia or hyperlipidemia.
How is diabetes diagnosed?
- A HbA1c of 48 mmol or above
- A random venous plasma glucose concentration >11.1 mmol/L
- A fasting plasma glucose concentration > 7.0 (6.1 whole blood)
- Two-hour plasma glucose concentration >11.1 mol/L two hours after 75g anhydrous glucose in an oral glucose tolerance test
How is gestational diabetes diagnosed?
- A fasting plasma glucose level of 5.6mmol/L or above
- A 2-hour plasma glucose level of 7.8mmol/L or above
- Risk factors include a previous gestational diabetes diagnosis, obesity, family history, south Asian ethnicity and previous enlarged baby
What is refeeding syndrome?
Refeeding Syndrome: is a metabolic disturbance that occurs as a result of reinstitution of nutrition in people and animals who are starved, severely malnourished or metabolically stressed because of severe illness. This presents with fatigue, weakness, confusion, hypertension, seizures, arrythmias and oedema. The electrolytes affected include potassium, magnesium and phosphate.
How do Biguanides work?
Reduces hepatic production of glucose by inhibiting gluconeogenesis and glycolysis. It also improves peripheral glucose uptake and utilisation.
How do sulphonylureas work?
Increases insulin production by binding to ATP K+ which depolarises the cell and causes Ca 2+ channels to open and insulin to be released
How do glitazones work?
These increase the actions of PPARy to promote adipogenesis and increase insulin sensitivity. The reduction of free fatty acids means the cells use the available glucose and hence lowers the concentration of glucose in the blood.
How do GLP-1 analogues work?
- Enhances GLP effect on the pancreas to increase insulin secretion
- Lowers gluconeogenesis
- Slows gastric emptying
- Inhibits inappropriate post prandial glucagon
- Increases peripheral glucose uptake
- Reduces satiety
How do DDP-4 inhibitors work?
DPP-4 enzyme normally breaks down incretins. Inhibitors mean incretins last longer. Also reduces the amount of glucagon secretion and decreases gastric emptying.
How do SGLT2 inhibitors work?
Prevents glucose reabsorption in the proximal tubules of the kidney.
They also promote weight loss and improve blood pressure.
What are the complications of reflux?
Benign structuring
Barrett’s
Problems related to achlorhydria – IDA, B12 deficiency from atrophic gastritis
When should faecal calprotectin be measured?
NICE recommends faecal calprotectin is used (in primary and secondary care) to investigate chronic diarrhoea. A low value is used to support a diagnosis of IBS. This test is not recommended in older patients because of the risk of missing serious pathology (false negatives) such as cancer.
What are the causes of Iron-deficiency anaemia?
A diet low in iron eg vegetarian/vegan
Malabsorption
Blood loss (think menorrhagia in women)
How should pyrexia of unknown origin be investigated?
Phase 1
Full hx and examination
FBC, WCC, blood film, U&Es, LFTs, bone profile, CRP, ESR, ferritin, TFTs
Blood culture and other cultures as appropriate
HIV screen
CXR and echo (if suspicion of endocarditis)
Following initial screen, other investigations ordered as dictated by clinical assessment and initial results
Phase 2
Immunoglobulins
Auto-antibody screen including anti-nuclear, anti-CCP and anti-neutrophil cytoplasmic antibodies
Serum protein electrophoresis and urinary Bence-Jones proteins
Lactate dehydrogenase
Serology for other infections : HBV, HCV, EBV, CMV, Toxoplasma, Coxiella, Bartonella
Imaging : CT of thorax, abdomen and pelvis,+/- PET as clinically dictated, transoesophageal echo (if transthoracic non-diagnostic)
Biopsy - liver, lymph node, bone marrow or other if indicated
NB - Bence -Jones proteins indicative of suggestive of multiple myeloma or Waldenström’s macroglobulinemia
What are the components of the Duke Criteria for endocarditis?
Modified Duke Criteria
Uses major or minor diagnostic criteria to diagnose endocarditis
A diagnosis of endocarditis can be made if the following are present;
2 major criteria
1 major criteria and 3 minor criteria, or
No major and 5 minor criteria
Major Diagnostic Criteria
Positive blood culture for typical infective endocarditis organisms from;
2 separate blood cultures or 2 positive cultures from samples drawn >12 hours apart
Or 3 or a majority of 4 separate cultures of blood (first and last sample drawn 1 hour apart)
Echocardiogram with oscillating intracardiac mass on valve or supporting structures, in the path of regurgitant jets, or on implanted material in the absence of an alternative anatomic explanation, or abscess, or new partial dehiscence of prosthetic valve or new valvular regurgitation
Single positive blood culture for Coxiella burnetii or anti-phase 1 IgG antibody titer >1:800
NB - typical infective endocarditis organisms include S. viridans or S. bovis, HACEK organisms, S. aureus without other primary site, Enterococcus
Minor Diagnostic Criteria
Predisposing heart condition or IVDU
Temp >38 degrees C
Vascular phenomena - arterial emboli, pulmonary infarcts, mycotic aneurysms, intracranial bleed, conjunctival haemorrhages, Janeway lesions
Immunologic phenomena - glomerulonephritis, Osler nodes, Roth spots, rheumatoid factor
Microbiological evidence: positive blood culture but does not meet a major criterion as noted above or serological evidence of active infection with organism consistent with endocarditis
Which organisms can cause endocarditis?
Most Common Organisms Causing Endocarditis
Staph aureus
Coagulase negative staphylococci (especially on prosthetic material)
Streptococcus viridans group
Streptococcus bovis group
Enterococci
HACEK organism
Others less commonly - Bartonella, Coxiella, chlamydia psittaci
Fungi in the immunocompromised
Describe treatment of endocarditis differ depending on the risk factors?
Endocarditis Management
Treatment of endocarditis is based on the susceptibility of the causative organisms and whether the infected valve is native or prosthetic
Intravenous antibiotics are required for several weeks to ensure sterilization of the endocardial lesions (vegetations)
For native valve endocarditis:
Streptococcal endocarditis is treated with benzylpenicillin +/- gentamicin for 2-6 weeks
Staphylococcus aureus is treated with flucloxacillin for at least 4 weeks
Enterococcus is treated with amoxicillin and gentamicin for 4-6 weeks
Surgery may be required where destruction of the valve causes complications, particularly in staphylococcal endocarditis
Define hospital acquired pneumonia
Hospital acquired pneumonia (HAP) is defined as a new presentation of a lower respiratory tract infection occurring at least 48 hours after admission to hospital, that was not clearly incubating at the time of admission
HAP vs CAP Organisms
CAP is commonly caused by gram-positive bacteria such as Streptococcus pneumoniae and Haemophilus influenzae
HAP is more likely to be caused by gram negative bacteria including Pseudomonas aeruginosa, Klebsiella pneumoniae, Eschericia coli, Enterobacter and Serratia and less commonly Staphylococcus aureus
How is hospital acquired pneumonia treated?
Any antibiotic regimen for HAP must provide coverage for gram-negative and possibly resistant organisms
Common choices include extended spectrum penicillins such as piperacillin-tazobactam or third generation cephalosporins such as ceftazidime or ceftriaxone
Other active agents to consider include fluoroquinolones (ciprofloxacin) and aminoglycosides (gentamicin or amikacin)
Carbapenems such as meropenem also have broad spectrum gram negative activity but are usually reserved for second-line use or for penicillin allergic patients
Where there are clinical features of staphylococcal pneumonia and/or known colonisation with MRSA, teicoplanin and/or linezolid may be added to the regimen
What is Clostridium difficile and how does it cause colitis?
Clostridium Difficile
A gram positive, anaerobic spore-forming bacterium that may be found in the bowel flora of approximately 3% of healthy adults
Spores may easily be transmitted via the faecal-oral route in healthcare environments
C difficile can proliferate in the colon when the normal flora is disturbed by the use of broad- spectrum antibiotics
It produces two high molecular weight toxins (A and B) which irreversibly glycosylate key Ras GTPases in human cells responsible for cell signalling, particularly in the cytoskeleton
This generalised cellular damage results in severe colonic inflammation and diarrhoea, with formation of the characteristic macroscopic pseudomembrane
How can antibiotic-associated diarrhoea, C. difficile colonisation and C. difficile colitis be distinguished?
Mild or moderate antibiotic-associated diarrhoea due to disturbances in the normal bowel flora is quite common during or after a course of broad-spectrum antibiotics and does not in itself signify C difficile infection
Clostridium Difficile Investigations
Glutamate dehydrogenase (GDH) test (detects the presence of C difficile specific antigen)
Detection of toxin gene (TG) by nucleic acid amplification (confirms toxigenic C difficile strain present)
Direct detection of toxin by immunoassay (confirms presence of toxins)
Interpretation of C. diff Investigations
GDH and/or TG negative – C difficile not present, toxin test not indicated
GD and/or TG positive, toxin negative – C difficile colonisation
GD and/or TG positive, toxin positive – C difficile colitis
How is C.difficile colitis treated and what are the outcomes?
Clostridium Difficile Colitis
Established agents for treatment of C difficile colitis include oral vancomycin, metronidazole and fidaxomicin given for 10-14 days
Relapse rates may be as high as 20% however and in severe cases surgical intervention including colectomy may be required
5% of patients die
New therapies including faecal transplant for recurrent cases are being developed
What are the potential complications of malaria?
Anaemia (due to haemolysis and hypersplenism)
Renal failure
Cerebral malaria
Acute Respiratory Distress Syndrome
Severe acidosis
Severe thromocytopenia, coagulopathy and bleeding
Plasmodium falciparum is the most commonly acquired species of malaria in travellers in the UK and is associated with sequestration of parasites in the capillary circulation, leading to organ damage
Malaria may be more severe in children, pregnant women and the elderly with less physiological reserve. Around 6 deaths from malaria occur in the UK each year
How is malaria treated?
Management of Acute Severe Malaria
Treated with intravenous artesunate (or with intravenous quinine if the former is not available) and appropriate supportive care
Less severe cases may be treated with a 3-day course of oral artemether-lumefantrine
Non-falciparum infections also need to be treated with primaquine to prevent relapse following hypnozoite formation in the liver
Advice for Travellers to Malarial Areas
Take standard precautions to avoid contact with mosquitoes using insecticide- impregnated bed nets, insect repellents and suitable clothing
Antimalarial chemoprophylaxis is also required, with current options including atovaquone/ proguanil, doxycycline or mefloquine
What are the causes of painless jaundice?
Hepatitis A – risk linked to faecal-oral spread when travelling
Hepatitis E – increasing in incidence. This has a high mortality in pregnant women
Hepatitis B
Hepatitis C – unusual – as a presentation: would require parenteral drug use / risk life
style
DILI – drug induced liver injury: drug side effects that harm the liver are common: co-amoxiclav is one of the more frequent causes. Flucloxacillin also a cause
Autoimmune disease – chronic active hepatitis / primary biliary cirrhosis /
Obstructive causes – Stones, Pancreatic cancer – rare but real
How should painless jaundice be investigated?
LFTs, viral serology, clotting tests, FBC, USS
Which viruses cause acute hepatitis?
A, B and E (and D)
What are the King’s college criteria for liver transplantation?
- Arterial pH < 7.3
- INR > 6.5
- Creatinine >3.4
- Grade III or IV hepatic encephalopathy
What are the 5 Fs of abdominal distention
Fat – obesity (is patient in denial and calling abdominal fat distension or bloating?)
Flatus
Fluid – ascites or cysts (eg ovarian cyst)
Faeces - constipation
Foetus – pregnancy
The ‘sixth’ would be flipping big masses
What does the appearance of the umbilicus in an abdominal exam tell you?
Deep/inverted - occurs with obesity
Protruding/everted/herniated - occurs with ascites
Flat - tends to occur with otters causes - flatus/faeces/foetus
What is paracentesis and why might it be useful?
Paracentesis is aspiration of ascitic fluid
Can be diagnostic (to aid diagnosis by looking - at the protein concentration,
- the white cells (for infection) and -cells types (cytology)
Can be therapeutic – removing fluid to relieve symptoms (discomfort from
distension and breathlessness from diaphragmatic splinting)
Broadly, ascites (like pleural fluid) can be an exudate (infection/malignancy) or a transudate (cirrhosis, cardiac failure, nephrotic syndrome)
Measure Serum Ascites Albumin Gradient (SAAG > or < 11g)
What are the complications of obesity?
Mechanical :
Pain, OA, Breathlessness, Obstructive Sleep Apnoea and Obstetric risk
Metabolic: T2DM, Vascular disease, NAFLD, Polycystic ovaries, Infertility and Hormone-dependent cancers
Psychosocial : Depression, Low income and Body image dysphoria
What are the causes of obesity?
Non-Medical Reasons for Obesity:
Eating more and less physical activity, Menopause and Metabolism slowing with age
Medical Reasons Causing Obesity:
Hypothyroidism
Insulin treatment in diabetes
Ageing – less muscle mass means less work so fewer calories burned
Steroid treatment
Cushing’s syndrome
Stress and low mood – turn to food as a coping mechanism
Lack of sleep
Fluid retention – eg. pre-menstrual, XS salt
Polycystic ovary syndrome
