Uworld- block 1 Flashcards
Most common causes of metabolic alkalosis
- Vomiting or nasogastric tube(hypotension)
- Thiazide or loop diuretics
- Mineralcorticoids excess(hypertension)
What are the most important steps in the workup of metabolic alkalosis
Checking the patients volume status and urine chloride
Differential diagnosis of metabolic alkalosis
In case of low chloride in urine: vomiting, nasogastric aspiration and prior diuretic use.
High chloride in urine: if euvolemia or hypovolemia are present -> bartter and gitelman syndromes
And if hypervolemia is present that means a status of excess mineralocorticoids
Which are saline responsive and unresponsive in treatment of metabolic alkalosis
Saline responsive : vomiting, nasogastric, diuretics
Saline unresponsive: barrter and gitelman syndrome, as well as excess mineralocorticoids.
Restlessness and purposeless jerking movement after a history of sore throat
Acute rheumatic fever -> sydenham chorea
Jerking extremity movement in Parkinson disease patients
Its seen only in case of levodopa intoxication
What is the role of thiamine in brain
Thiamine i a key coenzyme for pyruvate dehydrogenase which is involved in glucose metabolism. Its deficiency results in patients inability to metabolize glucose into energy. The most affected area in case of thiamine deficiency in the brain is the mammillary body( part of circuit of papez)
What is the character of inheritance for hemophilia a and b
X-linked recessive disorder
GRaft versus host disease (gvhd)
It can occur following transplantation of organs rich in lymphocytes.
This occur because the patients are severely immunodeficient due to immunosuppressant medications.
This is done via sensetization of T-cells and not B-cells.
GRaft versus host disease (gvhd) presentation
Any organ might be the target of this disease, but usually skin, liver , and gi tract are the most frequently affected. Early signs include a diffuse maculopapular rash the has predilection for palms and soles and may desquamate in severe cases.
Classification of MEN I
MEN I:
- Primary hyperparathyroidism.
- Pituitary tumors( prolactin, visual defects).
- Pancreatic tumors.
MEN II-A
MEN II-A:
- Medullary thyroid cancer(calcitonin).
- Pheochromocytoma.
- Parathyroid hyperplasia.
MEN II-B
MEN II-B:
- Medullary thyroid cancer
- Pheochromocytoma
- Mucosal neuromas, marfanoid habitus.
Thiamine is a cofactor for
- Pyruvate dehydrogenase
- A-ketoglutarate dehydrogenase
- Branched chain a ketoacid dehydrogenase
- Transketolase.
A deficiency in thiamine means that all these enzymes might not work prroporelly.
Chronic thiamine deficiency
If patients with chronic thiamine deficiency is given glucose infusion without thiamine supplementation, acute cereberal damage may occur. It can be diagnosed if baseline erythrocyte transketolase activity is low but increase after addition of thiamine pryiphosphate.
What is the most abundant amino acid in collagen
Glycine
Triple helix
The triple helical conformation of collagen molecules occurs due to the simple and repetitive amino acid sequence within each alpha chain in which glycine occupies every third amino acid position.
Proline in collagen
Proline residues are essential for alpha helix formation because of their ring configuration introduces a kink in the polypeptide chain, enhancing the rigidity oh the helical structure.
When does Hemoglobin F replaced b hemoglobin A
After 6 months.
Hemoglobin H diseaes
It manifests as chronic hemolytic anemia. It has 4 beta chains and its part of a-thalassemia. This have very high affinity for o2 that it doesnt release it.
Melanocyte embryonic derivative
Neural crest cell
Malignant melanoma can lead to
Focal neurological deficit which may manifest as tonic clonic seizures.
Most common cancers that lead to brain metastases
- Lung cancer
- Renal cancer
- Melanoma
Squatting in teratology of fallot- mechanismv
Squatting relieves tet spells. This posture increases systemic vascular resistance (important), without changing the pulmonary vascular resistance, increasing svr:pvr ratio. The increased svr forces a higher proportion of right ventricular output to enter the pulmonary circulation and oxygenate in the pulmonary capillary beds, increasing arterial oxygen concentration and relieving tet spell.