PBL Review Flashcards
What can be given as a treament for microcytic anaemia? [1]
What alternative can be given if first line treatment causes bad side effects? [1]
Oral iron: Ferrous sulphate.
Can give ferrous gluconate if side effects are bad
Name a disease that commonly causes Anaemia of chronic inflammatory disease [1]
rheumatoid arthritis
State two drugs that can cause B12 deficiency [2]
Name two autoimmune conditions that can cause B12 deficiency [2]
Drugs:
* Nitrous oxide
* Metformin
Autoimmune conditions:
* Crohns diease
* Pernicious anaemia
Describe the process of normal metabolism of B12 [7]
i. B12 broken down from protein
ii. Binds to haptocorrin in stomach
iii. Dissociates from haptocorrin
iv. Binds to stomach intrinsic factor
v. Absorbed in terminal ileum into blood
vi. In blood, binds with transcobalamin
vii. Stored in liver
Explain why assessing serum B12 levels may be deceptive [1]
B12 is either active or inactive in blood. Therefore may say have normal levels even though patient is deficient as they only have inactive B12
How do you calculate MCV? [1]
What is the unit [1]
MCV = Haematocrit / (Hb X RBC). It is expressed in femtolitres (fl) (1015 fl = litre)
Following haemorrhage there will be a what type of anaema in the short term? [1]
Explain your answer [1]
Following haemorrhage there will be a normocytic anaemia due to haemodilution, in the short term.
What serum markers would indicate someone is suffering from pernicious anaemia? [2]
- Antibodies to intrinsic factor
- Antibodies to gastric parietal cells occur in serum.
Which cell in the bone marrow differentiates into a common myeloid progenitor? (1 mark)
Haematopoietic stem cells
Which cells secrete intrinsic factor and where are they located? (1 mark)
Parietal cells [0.5] gastric mucosa [0.5]
How can reticulocytes be differentiated from erythrocytes on a blood film (1 mark).
Each point is worth half a mark
Reticulocytes are stained blue [0.5]
Reticulocytes bigger [0.5]
Ribosomes present [0.5]
How will the blood count of someone suffering from acute blood loss differ from someone suffering from chronic blood loss? (2 marks)
Acute: normocytic anaemia [1]
Chronic: IDA -> hypochromic microcytic anaemia [1]
Calculate a patient’s mean corpuscular volume, if their haematocrit = 0.45, Hb = 120 g/l, red cell count = 5 x 1012 /l (2 marks)
MCV = 0.45 / 5 x1012
= 90 fL
Heart Failure
Explain why the patient is breathless [1]
This is because the pulmonary venous pressure exceeds the oncotic pressures maintaining fluid within the pulmonary capillaries (cf Starling Principle). Breathlessness may then be due to inadequate transfer of oxygen from the alveoli to the blood.
Heart failure
Explain why the patient’s breathlessness is raised at night [3]
- This becomes exaggerated at night as the pulmonary venous pressure increases when someone is lying down and also because the respiratory drive is reduced during sleep.
- there is less sympathetic bronchodilation during sleep and this decreases oxygen diffusion into the alveoli.
- nerve endings in the lungs are activated and trigger an alarm reaction that wakes him up.
Heart failure
Explain the different lung sounds heard in the during heart failure [2
Crackles: bubbling or popping sounds that represent the presence of fluid or secretions, or the sudden opening of closed airways.
* Crackles that result from fluid (pulmonary edema) or secretions (pneumonia) are described as “wet” or “coarse,”
* Crackles that occur from the sudden opening of closed airways (atelectasis) are referred to as “dry” or “fine.”
Explain 5 symptoms of aortic stenosis [5]
i. Dyspnoea - increase in diastolic pressure in stiff non-compliant LV. LV is thicker because has to use more energy to expel blood (hypertrophy)
ii. Angina - increase O2 demand of hypertrophied LV
iii. Syncope - either paroxysmal ventricular arrhythmias or exertional cerebral hypoperfusion (less blood is leaving)
iv. LVF - contractile failure as ventricle dilates – causes heart failure
v. Sudden death - ventricular arrhythmias
What is the preferred imaging for aortic stenosis? [1]
Echocardiogram
What are the treatments for systolic heart failure? [9]
- ACE-Is (all grades of heart failure). Can cause dry cough.
- ARBs (if ACE-Is cannot be tolerated)
- beta-blockers (all grades of heart failure)
- spironolactone (NYHA grade III and IV only)
- Devices:
* cardiac resynchronization therapy (CRT) (pacemaker: causes two sides of heart to pump together – increases EF)
* ± ICD implanted cardiac defib: monitors heart rhythm – if goes into VF or VT, will give a shock into normal rhythm) - ARB/neprilysin inhibitor (neprilysin inhibits breakdown of BNP) (It includes the neprilysin inhibitor sacubitril (AHU377) and the ARB valsartan)
- SGLT-2 inhibitors (ESC guidelines 2021).
- Heart transplant
How does dilated cardiomyopathy lead to HF?
i. Causes nonsynchronous myocytes: impaired ventricular filling
ii. Decreases stroke volume
iii. Decreases cardiac output
iv. Increases preload
Acute LVF causes what type of lung failure? [1]
Type 1 resp. failure
Testing for BNP is sensitive but not specific. This means that when negative it is useful in ruling out heart failure, but when positive result
can have other causes. Other causes of a raised BNP include:? [5]
- Tachycardia
- Sepsis
- Pulmonary embolism
- Renal impairment
- COPD
Acute managment for LVF? [4]
Chronic HF management? [4]
ABAL
- ACE inhibitor (e.g. ramipril titrated as tolerated up to 10mg once daily)
- Beta Blocker (e.g. bisoprolol titrated as tolerated up to 10mg once daily)
- Aldosterone antagonist when symptoms not controlled with A and B (spironolactone or eplerenone)(spiro causes man boobs)
- Loop diuretics improves symptoms (e.g. furosemide 40mg once daily)
- What is the minimum number of days a patient with pneumonia may receive antibiotics? (1 mark)
Minimum duration of 5 days (1 mark)
Describe the pathophsyiology of asthma [4]
i. Allergen picked up by dendritic cells and presented by MHC Class II molecules
ii. CD4 cells activate the TH-2 lymphocytes through the release of IL4, IL5, IL13.
iII. IL 4 leads to the production of IgE antibodies: coat mast cells and stimulate degranulation and the release histamines, leukotrienes and prostaglandins
iv. IL-5 activates eosinophils: causes more cytokine & leukotrienes release
v IL-9 = mast cell proliferation
Describe the difference in IL-5 and IL-9 in asthma pathophysiology [2]
- IL-5 = Eosinophil activation
- IL-9 = mast cell proliferation
Describe the symptoms of asthma [5]
Episodic symptoms:
ii. Diurnal variability. Typically worse at night.
iii. Dry cough with wheeze and shortness of breath
iv. A history of other atopic conditions such as eczema, hayfever and food allergies
vi. Bilateral widespread “polyphonic” wheeze heard by a healthcare professional. BUT: neither sensitive nor specific for asthma
vii. Prolonged expiratory phase (respiratory and expiratory phases should be equal)
Describe asthma treatment pathway
Reliever medication: Short acting beta 2 agonists (SABAs)
1. Adrenalin acts on the smooth muscles of the airways to cause relaxation.
2. This results in dilatation of the bronchioles and improves the bronchoconstriction present in asthma
First line therapy:
* Low dose inhaled ICS (if need, may required higher doses)
Add on therapy:
* ICS + inhaled long acting beta 2 agonists (LABA) or long acting anti muscarinic (LAMA)
Add on therapy:
ICS + LAMA / LABA + specialist therapies
What is MART / SMART therapies? [1]
is a form of combined ICS and LABA treatment in which a single inhaler, containing both ICS and a fast-acting LABA, is used for both daily maintenance therapy and the relief of symptoms as required.
ICS causes a reduction in why three pro-inflammatory mediators in asthma? [3]
IL-6, TNF-a & CXCL8
Describe the management for mild, moderate and severe pneumonia [3]
i. Mild CAP: 5 day course of oral antibiotics: amoxicillin or a macrolide (azithromycin)
ii. Moderate to severe CAP: 7-10 day course of dual antibiotics (amoxicillin AND macrolide (azithromycin)
iII Severe Benzylpenicillin if blood culture tells you something different
What is ‘silent chest’ in life threatening asthma? [1]
- No wheeze. This occurs when the airways are so tight that there is no air entry at all. This is ominously described as a “silent chest”.
What are the PEFRs for:
Moderate
Severe
Life-threatening asthma
Moderate: 50-75% predicted
Severe: 33-50% predicted
Life-threatening asthma: < 33%
Acute asthma management? [5]
O! SHIT!
Oxygen
Salbutamol - (? in cardiac patients with presenting tachy, monitor potassium!)
Hydrocortisone - (or any steroid)
Ipratropium Bromide - (acetylcholine antagonist via blockade of muscarinic cholinergic receptors)
Tube (intubation) - (only if VVV severe)
Magnesium (calcium channel blockade)
First line investigations for asthma diagnosis? [2]
Second line? [2]
First line
* Fractional exhaled nitric oxide
* Spirometry with bronchodilator reversibility
Second line
* Peak flow variability measured by keeping a diary of peak flow measurements several times per day for 2 to 4 weeks
* Direct bronchial challenge test with histamine or methacholine
Characteristic chest signs of pneumonia? [3]
Bronchial breath sounds. These are harsh breath sounds equally loud on inspiration and expiration. These are caused by
consolidation of the lung tissue around the airway.
Focal coarse crackles. These are air passing through sputum in the airways similar to using a straw to blow in to a drink.
Dullness to percussion due to lung tissue collapse and/or consolidation.
Describe the MoA of amoxicillin [1]
Amoxicillin competitively inhibit penicillin binding proteins, leading to up-regulation of autolytic enzymes and inhibition of cell wall synthesis.
Describe the MoA of Macrolides [2]
Macrolides inhibit bacterial protein synthesis.
The mechanism of action of macrolides revolves around their ability to bind the bacterial 50S ribosomal subunit causing the cessation of bacterial protein synthesis.
Name an ICS used to treat asthma [1]
Beclomethasone
What is pabrinex and explain which pathology it may prevent by providing it [2]
Pabrinex: provides additional vitamins B and C to correct deficiencies that may have occurred. Incudes Thiamine. Thiamine deficiency can lead to Wernicke Encephalopathy
Desribe the action (and site of action) of terlipressin
- Terlipressin: is a synthetic analogue of vasopressin, which is an endogenous neurohormone that acts as a vasoconstrictor – maintains pressure for the kidneys
How do you treat Hepatic Encephalopathy? [1]
Lactulose: clears toxins from your blood by leading to frequent bowel movements, with less time for ammonia absorption and increased fecal nitrogen excretion.
Describe the pathophysiology of cirrhosis [3]
State 4 disease it can lead to [4]
Hepatic fibrosis leads to cirrhosis with nodule formation. Prevents regeneration
* Activation of hepatic stellate cells: cause accumulation of collagen type I and III in the hepatic parenchyma and space of Disse
* Stellate cells also become more contractile
* Accumulation of collagen causes altered exchange between hepatocytes and plasma
* Disrupts blood flow and causes increased pressure in the portal venous system: portal hypertension, causing:
i. Ascites
ii. Gastro-oesophageal varices
iii. Rectal varices
iv. Promotes the diversion of nutrient carrying blood away from the liver and cause hepatic encephalopathy
Explain the results
Low Hb, Low plts and High INR: liver disease causes coagulation disorder leading to bleeding and subsequent anaemia.
Low albumin: the liver makes less albumin leading to deviations of the equilibrium between osmotic pressure and hydrostatic pressure in the blood vessels. Low albumin along with portal hypertension, results in the patient suffering from ascites and oedema. Albumin is also a marker of nutritional status.
High bilirubin: bilirubin (waste product from the breakdown of RBC). The liver has reduced ability to conjugate bilirubin, so it can’t be excreted, leading to high levels being present in blood. This causes jaundice
.
High ALP, AST, ALT and GGT: these liver enzymes are present at higher levels in the blood when leaking out of dying hepatocytes. Not extremely as liver was previously damaged by HCV.
High urea: main nitrogenous breakdown product of protein metabolism. High urea due GI bleeding being digested as a “protein rich meal”.
Low end of normal glucose: liver is unable to maintain blood glucose level due to damage.
Explain the consequences of liver failure on the metabolic state [2]
Which energy store is the patient with decompensated liver most likely using as main energy supply? [1]
(There are similarities to the starved state here)
- Blood glucose is on the low side and this is symptomatic of the liver not being able to store glycogen/do glycogenolysis and gluconeogenesis thus blood glucose homeostasis will be impaired.
- Similarly, ketones are unlikely to be as high as they would if the liver was fully functioning. In this case, the patient is likely to be using fats as their main energy supply.
Explain why gallstones made lead to a prolonged INR? [1]
Lack of bile salts gives malabsorption of fats and slows absorption of fat-soluble vitamin K, which is required for synthesis of some clotting factors including prothrombin.
A portal pressure above [] mmHg causes portal hypertension? [1]
Pressure rise above 14 mmHg (usual: 5-10 mmHg)
Explain why hepatic encephalopathy is a complication of liver cirrhosis [3]
Ammonia: the liver clears almost all of the portal vein ammonia, converting it into glutamine and urea, preventing entry into the systemic circulation. Ammonia is a by-product of the metabolism of nitrogen-containing compounds, and is neurotoxic at elevated concentrations.
GI bleeding: the presence of blood in the upper GI tract results in increased ammonia and nitrogen absorption from the gut.
Aromatic amino acids (AAA): the increase in plasma AAA, resulting from a change in the** ability of the liver to process them** has been suggested to contribute to an increased influx in the brain leading to imbalances in neurotransmitter synthesis.
Explain why spontaneous bacterial peritonitis is a complication of liver cirrhosis [2]
Weakened immune system
- The liver contains 90% of the reticuloendothelial (RE) cells, such as Kupffer and sinusoidal endothelial cells, which are central to clearing bacteria.
- Most of the proteins of the “complement system” (part of the immune system that enhances the ability to clear microbes) are made by the liver. This increases the risk of bacterial peritonitis and thus the need for antibiotics
3) (i) What role does the liver plays in immunity? (ii) Why is the patient at risk of infection? [2 marks]
Weakened immune system due to reduction in energy metabolism, reduced formation of complement system protein, compromised reticuloendothelial function (Kupffer cells etc…) [1 mark].
Build-up of fluid increases risk of infection (providing a perfect 37C niche for bacterial growth) [1 mark]
5) Pabrinex, Lactulose and terlipressin are all part of the treatments for decompensated liver cirrhosis: describe their mode of action. [3 marks]
Pabrinex
* (via intravenous injection) provides these: mix of B vitamin (essential for a range of bodily processes and form part of the co-enzyme involved in carbohydrate, protein and lipid metabolism). (i) Thiamine is an important co-factor for the conversion of Pyruvate to AcetylCoA (which feeds into the Krebs cycle). If Thiamine is lacking, then Pyruvate forms lactic acid instead (which is neurotoxic).
Pabrinex also contain glucose, as the liver has impaired gluconeogenesis. [1 mark]
Lactulose - By acidifying the contents of the gut, lactulose reduces the absorption of ammonia from the gut, thereby helping to prevent encephalopathy. [1 mark]
Terlipressin - (analogue of vasopressin). It is important to reinstall correct blood circulation and support kidney function. (Main factors in the pathophysiology of hepatorenal syndrome are splanchnic vasodilation and increased cardiac output).
[1mark]
Describe mode of transmission for Hep A [1] and Hep B viruses? [1]
Hep A: faecal-oral route (contanimated water)
Hep B: Blood bourne / vertical transmission
What are normal kPa fibroscan scores? [1]
2-7kPa is normal, highest is 75
The four most common causes of liver cirrhosis are? [4].
- Alcoholic liver disease
- Non Alcoholic Fatty Liver Disease
- Hepatitis B
- Hepatitis C
What is a tumour marker for hepatocellular carnicoma? [1]
Alpha-fetoprotein is a tumour marker for hepatocellular carcinoma and can be checked every 6 months as a screening test in patients with
cirrhosis along with ultrasound.
Which drug reduces the number of intestinal bacteria producing ammonia? [1]
rifaximin
Which HLA do most type 1 diabetic patients have? [2]
HLA-DR3-DQ2 or HLA-DR4-DQ8
What are the 3Ps of symptoms of type 1 diabetes? [3]
Polyuria (lots of urine)
o Glucose draws water into the urine by osmosis - not enough glucose can be reabsorbed as kidneys have reached the renal maximum reabsorptive capacity
o Can cause bed wetting
Polydipsia (extreme thirst)
o Due to high water loss due to XS glucose and water loss
Polyphagia (extreme appetite)
o Weight loss due to lipolysis in adipose tissues and break down of muscle protein because glucose is lost
What are the random [1] and fasting [1] plasma glucose levels that would indicate type 1 diabetes?
Random plasma glucose:
* > 11.1 mmol/L
Fasting plasma glucose:
* ≥7.0 mmol/L
Explain the consequence of insulin deficiency on glucose levels [3]
Explain the consequence of insulin deficiency on ketone body levels [2]
TN
Glucose
* Glycogen breakdown stimulated
* Gluconeogenesis stimulated
* Decreased removal of glucose by peripheral tissues
Ketone bodies
* Increased activity of acetyl CoA undergoing B-oxidation of fatty acids in liver
* Causes an increase (in acetoacetate; which leads to more) acetone
Describe the mechansim of diabetic ketoacidosis [5]
- Uncontrolled breakdown of glycogen & increased GNG due to lack of insulin; causes hyperglycaemia and therefore glycosuria
- Glycosuria causes osmotic diuresis; loss of electolytes and water
- Lipolysis; causing ketone bodies acetoacetate and 3-hydroxybutyrate ionised; results in an accumulation of ketone bodies; increased pH
- Some unionised acetoacetic and 3-hydroxybutyric acids are excrete in urine
- Increased pH can cause enzyme degradation, CNS depression, cerebral oedema and coma
What is the name for the characteristic breathing in DKA? [1]
What speficially causes this symptom? [1]
Kussmauls respiration: rapid deep breathing
Stimulation of H+ on the medullary resp. centre
Why is HCO3- low in DKA? [1]
Excess hydrogen ions bind the bicarbonate, resulting in decreased serum bicarbonate levels
Acidosis in DKA is due to the overproduction of which two molecules? [2]
Acidosis in DKA is due to the overproduction of β-hydroxybutyric acid and acetoacetic acid
( At physiological pH, these 2 ketoacids dissociate completely)
What mmol/L of blood ketones would indicate DKA? [1]
> 3.0mmol/L
What levels of HCO3- would indicate DKA? [1]
< 7.3 mmol/L
What is a possible consequence of not monitoring K+ levels in DKA management? [1]
How can you avoid this? [1]
o Hypokalaemia is important because when give insulin drives glucose and K into the cell; Large scale: cause cardiac arrythmias
Manage: Supply K at the same time as insulin
To diagnose DKA you require [3]
Hyperglycaemia (i.e. blood glucose > 11 mmol/l)
* Ketosis (i.e. blood ketones > 3 mmol/l)
* Acidosis (i.e. pH < 7
Causes of a normal anion gap or hyperchloraemic metabolic acidosis? [5]
Causes of a raised anion gap metabolic acidosis? [5]
Management for C. trachomatis [2]
- Doxycycline everyday for a week
- Azithromycin once a day for three days
Describe the test used to diagnose C. trachomatis [1]
ii. Positive nucleic acid amplification test (NAAT; checks directly for RNA or DNA of organism)
1. Vulvovaginal swab
2. Endocervical swab
3. First catch urine sample
4. Urethral swab in men
5. Anal swab
6. Pharyngeal swab
What is the most common cause of PID? [1]
i. Chlamydia trachomatis
How do you diagnose PID? [3]
i. Elevated white blood cell count
ii. Presence of polymorphonuclear cells on vaginal smear
iii. Genetic probe / culture of vaginal secretions for chlamydia or gonorrhoea
Know this
Management of PID [3]?
i. Parenteral cephalosporin & oral doxycycline & oral metronidazole
Describe the MoA for:
- Parenteral cephalosporin
- oral doxycyclin
- oral metronidazole
Cephalosporin:
* The beta-lactam rings bind to the penicillin-binding protein and inhibit its normal activity. Unable to synthesize a cell wall, the bacteria die
Doxycycline:
* allosterically binding to the 30S prokaryotic ribosomal unit during protein synthesis
metronidazole
* binds deoxyribonucleic acid and electron-transport proteins of organisms, blocking nucleic acid synthesis
Signs and symptoms of ectopic pregnancy? [6]
- Missed period
-
pain in the tip of your shoulder
a. Sign that this pain is caused by blood leaking into the abdomen and is a sign that the condition is getting worse - Constant lower abdomen pain in right or left iliac fossa
- Vaginal bleeding
- Lower abdomen tenderness
- Cervical motion tenderness (pain when moving cervix in bimnaul exam)
- Palour
Describe the treatment plan for ectopic pregnancy if requires:
Expectant management
Medical managment
Surgical management
-
Expectant management
a. Await natural termination
b. Needs to not ruptured
c. No significant pain
d. No visible heartbeart -
Medical management
a. IM Methotrexate (in buttock)
i. Need to have oral contraceptives 3 months after treatment because is tetragenic) -
Surgical management (if tube has ruptured)
a. Laparoscopic salpingectomy
b. Laparoscopic salpingotomy
Name the two of the three complications of pelvic inflammatory disease and the reason that this arises. (3 marks)
Any 2 from
Chronic pelvic pain (0.5 marks) : This pain is thought to be related to cyclic menstrual changes, but it also may be the result of adhesions or hydrosalpinx. (1 mark)
Infertility (0.5 marks): Infection and inflammation can lead to scarring and adhesions within tubal lumens. The rate of infertility increases with the number of episodes of infection. (1 mark)
Ectopic pregnancy (0.5 marks): Ectopic pregnancy is a direct result of damage to the fallopian tube. (1 mark)
Explain why transvaginal ultrasound is the preferred imaging modality for early pregnancy monitoring. (2 marks)
By inserting the ultrasound wand into the vagina it provides a better view of the reproductive organs and the contents of the uterus as it is closer to the structures (1 mark)
and the ultrasound waves do not have to travel through the abdomen (1 mark)
What is the mode of action of methotrexate in this case? (2 marks)
Its mechanism of action, competitive inhibition of folate-dependent steps in nucleic acid synthesis, (1 mark) effectively kills the rapidly dividing ectopic trophoblast. (1 mark)
( if the student puts Methotrexate works by blocking the enzymes in the body that maintain the pregnancy. It stops the tissue from growing bigger and prevents it from rupturing (bursting). The pregnancy tissue is then gradually reabsorbed by the body. (1 mark) only)
Which organism causes more severe PID? [1]
- Neisseria gonorrhoeae tends to produce more severe PID
- A 27 year old woman who is 12 weeks pregnant attends the antenatal clinic for the results of her nuchal translucency scan and serum screening tests. The results reveal she has an increased nuchal translucency and decreased pregnancy-associated plasma protein A (PAPP-A) levels. What is the single most appropriate intervention at this point and why? (3 marks)
Chorionic villus sampling (1 mark)
Her results indicate a risk of her baby having Down syndrome (1 mark)
CVS would give a definitive diagnosis via karyotyping (1 mark)
Describe the pathophysiology of colon cancer [1]
Majority arise from dysplastic adenomatous polyps
Describe the differences between D1 and D2 receptor inputs to the direct and indirect pathways
Describe the pathophysiology of Parkinson’s disease [4]
Explain the results table
Explain results table: ALP raised osteoblasts are making more of enzyme. Low 25 (OHD) suggests that not absorbing much calcium from gut, so increased extraction from bones. Ca is normal so PTH is also normal
X-rays often do not show any changes, particularly in early disease.
They cannot be used to exclude osteomyelitis. The potential signs of osteomyelitis on an x-ray are: [3]
Periosteal reaction (changes to the surface of the bone)
Localised osteopenia (thinning of the bone)
Destruction of areas of the bone
State what the following mean with regards to imaging of osteomyelitis:
Sequestrum [1]
Involucrum [1]
Cloaca [1]
Sequestrum: Refers to a dead piece of devitalised bone that has been separated (i.e. sequestered) due to necrosis from the surrounding bone.
Involucrum: New growth of periosteal bone around a sequestrum.
Cloaca: An opening in an involuvcrum that allows the internal necrotic bone and pus to discharge out.
Name and explain this sign of Pott’s disease? [1]
Pott’s Disease Cold Abscess: abscesses typically lack all the inflammatory signs obvious in abscesses
Describe the role of T3 at the liver [2] and at peripheral tissues [2]
-
Opposes insulin at liver: Long term changes because they effect gene expression
a. Increased glucose intestinal absorption
b. Increases hepatic GNG - **Mimics insulin at peripheral tissues / muscle **
a. Upregulates GLUT4
b. Increased glycolysis
How do you diagnose Addisions?
Synacthen is another name for tetracosactide, the chemical used in the test.
ACTH is the chemical (hormone) released by your pituitary gland, which stimulates the adrenal glands to produce cortisol. If the adrenal glands are working properly they should respond to the tetracosactide by producing cortisol. Levels of cortisol are checked by taking a blood sample.
If levels of cortisol remain low, despite the tetracosactide injection, this suggests there is a problem with the function of the adrenal glands
Describe the role of obesity causing DMT2
