True hypokalemia may result from one or more of the following: (1) decreased net intake, (2) shift into cells, or (3) increased net loss.
Diminished intake is seldom the sole cause of K+ depletion because urinary excretion can be effectively decreased to <15 mEq/d. However, dietary K+ restriction may exacerbate the hypokalemia from GI or renal loss.
Transcellular shift. Movement of K+ into cells may transiently decrease the plasma [K+] without altering total body K+ content. These shifts can result from alkalemia, insulin, and catecholamine release.
Hypokalemic periodic paralysis is a rare disorder that predisposes patients to transcellular K+ shifts that result in episodic muscle weakness. The hypokalemic form can be triggered after a carbohydrate-rich meal.
Nonrenal K+loss. Hypokalemia may result from the loss of potassium-rich fluids from the lower GI tract. Hypokalemia from the loss of upper GI contents is typically more attributable to renal K+ secretion from secondary hyperaldosteronism. Rarely, in excessive sweating, loss of K+ through the integument can provoke hypokalemia.
Renal K+loss accounts for most cases of chronic hypokalemia. This may be caused by any of the following factors:
Augmented distal urine flow occurs commonly with diuretic use and osmotic diuresis (e.g., glycosuria).
Hyperaldosteronism can result in increased renal K+ loss because aldosterone plays a central role in coupling the reabsorption of sodium with the excretion of potassium.
Ref Washington manual of surgery
Q2) Loss of cell surface antigen is a feature of A. CIS B. NO RELATION WITH GRADE C. LOW GRADE TUMOR D. HIGH GRADE TUMOR
Ans2 d High grade
The ABO(H) blood group system consists of terminal oligosaccharide antigens carried by glycoproteins or glycolipids in hematopoietic or epithelial cells
Their biosynthesis is presumed to be controlled by the ABO(H), Se, H, Le, and X blood group genes .
These antigens are present on normal bladder epithelium of secretor individuals but not on some low-grade and early-stage papillary urothelial carcinomas
Moreover, initially expressing tumours lose these cell surface antigens upon local recurrence, progression to invasion or metastization
Q3) For carcinoma of unknown primary with no lesion found on clinical examination,
A.blind biopsies detect primary 40% times
B.tonsillectomies find primary 20% times
c.PET find primary 60% times
d.CXR finds primary 20% times
PET is more sensitive than CT in identifying the primary lesion but cannot detect unknown primary tumors with more than 50% sensitivity
Q4. Not a definition under RECIST criteria,
a.>20mm , on CXR
b.>10mm , on CT,5mm cuts
c.>20mm , on USG
d.>20mm , on CT,10mm cuts
Ans 4 d
Measurable Tumour lesions: Must be accurately measured in at least one dimension (longest diameter in the plane of measurement is to be recorded) with a minimum size of: • 10 mm by CT scan (CT scan slice thickness no greater than 5 mm) • 10 mm caliper measurement by clinical exam (lesions which cannot be accurately measured with calipers should be recorded as non-measurable). • 20 mm by chest X-ray
lymph node must be P15 mm in short axis when assessed by CT scan (CT scan slice thickness recommended to be no greater than 5 mm)
Q5) Most common cause of Superior Vena Cava (SVC) syndrome
A. Non neoplastic B. Lung ca C. Breast ca
Ans 5 b
SVC obstruction is complete or partial block in flow through SVC.
Could be due to intraluminal thrombus or external tumor compression.
Etiology - Most common is Malignancies but recently rise in benign causes.( 40%)
Mediastinal malignancies, primary among which is small cell bronchogenic carcinoma
NON hodgkin lymphoma
Management is Treatment of cause and endovascular recanalization