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RENAL
SYSTEM
Dr. Md Abdul Hamed Jasham
FCPS(Part I) (Internal Medicine)
MD(Phase-A) (Critical Care Medicine)
Banghabandhu Sheikh Mujib Medical University
 Topics tobe covered
• Structure and Function of kidney
• Hormone produced from kidney
• Renal circulation, RBF
• Agents causing contraction or relaxation of mesangial cells
Juxtaglomerular apparatus (JGA)
Glomerular membrane and filtration
• Factory affecting GFR
• Reabsorption & Secretion: PCT, TAL, DCT, CD
Sites of Sodium, Potassium, Water reabsorption
Mechanism of urine concentration
• Acidification of urine and bicarbonate excretion
• Hormones acting on Kidney with effect
• RAAS: Functions of Angiotensin II
 Topics tobe covered
• Body response to Hypovolemia/ Hypervolemia/Hypertonicity
• RTA
• Metabolic acidosis: (high and normal anion gap)
• Respiratory Acidosis: Cause and systemic effect
• Respiratory Alkalosis (Hyperventilation): Biochemical Changes
• Hypernatremia + Hyponatremia: Causes
• Hyperkalemia+ hypokalemia
• Hypocalcaemia: Causes and features
• Hypercalcaemia: Causes
01. Following parts of a juxta medullary nephron
present in cortex-
a) PCT
b) ALLH
c) DLLH
d) DCT
e) CD
Structure & Functions of the kidneys
Nephron: Nephron is the structural and functional unit
of kidney. Each human kidney comprises about 1 million
nephrons.
 
Classification of nephrons: Two types –
1. Cortical nephrons (85%):
The glomeruli of these nephrons are located in the
outer cortex just under the capsule. They have short
loop of Henle.
2. Juxtamedullary nephrons (15%):
The glomeruli of these nephrons are located deep to
the cortex near the medulla. They have long loop of
Henle.
Difference between cortical and juxta medullary
nephron

Feature Cortical Juxta

nephron medullary
nephron
Number 80-85% of total 15-20% of total
Situation of Outer cortex Inner cortex near
glomerulus medulla
Loop of Henle (LH) Short Long
Extension of LH Not beyond outer Deep into
medulla medulla
Vasa recta Absent Present
Involvement with Not involved Involved
counter current
mechanism
01. Following parts of a juxta medullary nephron
present in cortex-
a) PCT
b) ALLH
c) DLLH
d) DCT
e) CD
TFFTF
02. Following cells present in Juxta glomerular
apparatus-
a) Capillary endothelial cell
b) Lacis cell
c) JG cell
d) Polkissen cell
e) Podocyte
02. Following cells present in Juxta glomerular
apparatus-
a) Capillary endothelial cell
b) Lacis cell
c) JG cell
d) Polkissen cell
e) Podocyte
FTTTF
03. Hormones secreted by kidneys are
a) Erythropoietin
b) Thromboxane
c) Vasopressin
d) Renin
e) 1,25dihydroxycholecalciferols
 Functions of kidney
Endocrine functions:
1. Formation of Erythropoietin is response to hypoxia.
2. It secretes renin, which converts angiotensinogen to angiotensin-1.
3. Angiotensinogen Renin Angiotensin-1
Formation of active form of vitamin D: 1,25 dihydroxycholecalciferol [ 1,25
(OH)2D3] under the influence of parathyroid hormone.
4. It also produces Prostaglandin (PG): PGI2, PGE2 synthesized by messangial
cells of glomeruli & interstitial cells of medulla, PG causes vasodilation &
increases renal blood flow.
5. EDRF or NO.
  
Metabolic function:
Transamination & deamination of amino acids occur in kidney.
03. Hormones secreted by kidneys are
a) Erythropoietin
b) Thromboxane
c) Vasopressin
d) Renin
e) 1,25dihydroxycholecalciferols
TFFTT
04. Renal blood flow-
a) 10% of cardiac output
b) Renal blood flow autoregulation by sympathetic system
c) Angiotensin II Decreases renal blood flow.
d) Prostaglandin increases renal blood flow
e) Blood supply more in renal cortex than medulla)
Peculiarities of RBF with their importance

1.It is a portal system containing two sets of

capillaries.
▪ Glomerular capillary- It is designed for filtration of
plasma.
▪ Peritubular capillary- It is designed for the secretion or
reabsorption of desirable substances from the filtrate.

2. Kidney has a high-Pressure capillary bed. Renal artery

is a direct branch of abdominal aorta, which is a high-
pressure artery. Hydrostatic pressure in the glomerular
capillary (60 mm of Hg). On the other hand, in a classic
microcirculation, hydrostatic pressure at the arterial end of
capillary is only 35 mmHg.
 
 
3. Rate of blood flow to kidney is very high (4ml/gm of
kidney tissue/min): RBF is four times of the blood
flow to liver and eight times of the blood flow to
heart .

4. Blood flow is selective, not uniform. 98-99% of

renal blood flow goes to cortex and 1-2% to
medulla. Maximum, about 100% glomerular capillary
lies in cortex. So blood flow in cortex is very high.
 
 5. Auto regulation of RBF by kidney itself. It is the
intrinsic capacity of kidney to maintain renal blood flow
and GFR relatively constant so long as the mean
systemic blood pressure remains within the range of 80-
180 mmHg.
▪ At blood pressure below 80 mmHg, autoregulation fails
and GFR gradually decreases with decreasing blood
pressure to cause oliguria or anuria.
▪ At blood pressure above 180 mmHg, autoregulation
fails and GFR gradually increases with increasing blood
pressure to cause polyuria (Pressure dieresis)
 
 
6. Renal blood flow is not altered in denervated or
innervated kidney.
 
7. Presence of vasa recta: In the vasa recta,
velocity of blood flow is very slow and direction of
blood flow is antiparallel.

Importance: This helps to create & preserve

medullary hyperosmolarity.
04. Renal blood flow-
a) 10% of cardiac output
b) Renal blood flow autoregulation by sympathetic system
c) Angiotensin II Decreases renal blood flow.
d) Prostaglandin increases renal blood flow
e) Blood supply more in renal cortex than medulla)
FFTTT
05. In the glomerular filtration system
a) The basal laminae of the glomerular capillary and podocytes fuse
b) The capillary has fenestrations (pores) in between the
endothelial cells
c) The podocyte processes interdigitate
d) Electrical charge of the membrane determines the nature of
filtration
e) The mesangial cells play a key role
05. In the glomerular filtration system
a) The basal laminae of the glomerular capillary and podocytes fuse
b) The capillary has fenestrations (pores) in between the
endothelial cells
c) The podocyte processes interdigitate
d) Electrical charge of the membrane determines the nature of
filtration
e) The mesangial cells play a key role
TTTTT
06. Factors increasing GFR are
a) Increase in glomerular capillary hydrostatic pressure
b) Sympathetic stimulation
c) Increase in plasma colloid osmotic pressure
d) Afferent arteriolar dilatation
e) Efferent arteriolar constriction
06. Factors increasing GFR are
a) Increase in glomerular capillary hydrostatic pressure
b) Sympathetic stimulation
c) Increase in plasma colloid osmotic pressure
d) Afferent arteriolar dilatation
e) Efferent arteriolar constriction
TFFTT
07. Factors that cause an increase in both glomerular
filtration rate and renal plasma flow are
a) Ureteral stone
b) Dilatation of afferent arteriole
c) An increase in filtration coefficient
d) Constriction of the efferent arteriole
e) Prostaglandins E2
 Hormones or Action Effects
Autacoids
Epinephrine & Constriction of afferent & 🡫GFR
norepinephrine efferent arteriole 🡫Renal blood flow
Endotheline Constriction of afferent & 🡫 GFR
efferent arteriole
Endothelium-derived Prevent excessive 🡩 GFR
No vasoconstriction in afferent &
efferent arteriole
Angiotensin-II 🡫 GFR
Prostaglandin Vasodilation of afferent & 🡩GFR
efferent arteriole 🡩Renal blood flow
Bradykinin Vasodilation of afferent & 🡩GFR
efferent arteriole 🡩Renal blood flow
Constriction of efferent arteriole:
•Moderate constriction 🡪🡩 resistance to out flow of
blood from glomerular capillary 🡪🡩 glomerular
hydrostatic pressure 🡪🡩 GFR slightly.
• Severe constriction 🡪 accumulation of blood in the
glomerulus for a long time 🡪🡩 protein conc. in
glomerular capillary 🡪🡩 glomerular capillary colloidal
osmotic pressure 🡪🡫 GFR.
07. Factors that cause an increase in both glomerular
filtration rate and renal plasma flow are
a) Ureteral stone
b) Dilatation of afferent arteriole
c) An increase in filtration coefficient
d) Constriction of the efferent arteriole
e) Prostaglandins E2
FTTFT
08. Agents causing relaxation of mesangial cells-
a) ANP
b) Angiotensin II
c) Dopamine
d) Norepinephrine
e) Vasopressin
08. Agents causing relaxation of mesangial cells-
a) ANP
b) Angiotensin II
c) Dopamine
d) Norepinephrine
e) Vasopressin
TFTFF
09. Renin Angiotensin Aldosterone system:
a) Renin is converted to Angiotensin I in kidney
b) Angiotensin II is an arterial vasoconstrictor
c) Hyperadosteronism causes alkalosis
d) Hypovolaemia stimulates renin release
e) Aldosterone acts on membrane receptor on collecting duct
Hypovolumia
Hypotension
Symp.

Pulmonary capillary
endo
Aldosterone
ADH
Stimulates thrist center
09. Renin Angiotensin Aldosterone system:
a) Renin is converted to Angiotensin I in kidney
b) Angiotensin II is an arterial vasoconstrictor
c) Hyperadosteronism causes alkalosis
d) Hypovolaemia stimulates renin release
e) Aldosterone acts on membrane receptor on collecting duct
FTTTF
10. Renin secretion is increased in
a) Essential hypertension
b) Over hydration
c) Sodium depletion
d) Diuretic therapy
e) Renal artery stenosis
10. Renin secretion is increased in
a) Essential hypertension
b) Over hydration
c) Sodium depletion
d) Diuretic therapy
e) Renal artery stenosis
FFTTT
11. Following substances are completely reabsorbed
from renal tubules:
a) HCO3-
b) Glucose
c) H20
d) Vitamin
e) Amino acid
11. Following substances are completely reabsorbed
from renal tubules:
a) HCO3-
b) Glucose
c) H20
d) Vitamin
e) Amino acid
FTFTT
12. Freatures of proximal convoluted tubules-
a) Reabsorbs 40% of filtered Na+
b) Reabsorption of 〖 HCO_3 〗 ^-
c) Secretion of P 〖 O_4 〗 ^(3-)
d) Site of action of PTH
e) Site of action of triamterene
12. Freatures of proximal convoluted tubules-
a) Reabsorbs 40% of filtered Na+
b) Reabsorption of 〖 HCO_3 〗 ^-
c) Secretion of P 〖 O_4 〗 ^(3-)
d) Site of action of PTH
e) Site of action of triamterene
FTFTF
13. Na+ can be transported across the luminal
membrane of renal tubular cells by
a) Co-transport with organic solutes
b) Sodium potassium ATPase system
c) Sodium channels
d) Counter transport with H+
e) Counter transport with Ca++
1. Na+-X symporter (here “X” represents glucose or
amino acid or phosphate)
2. Na+ - H+ antiporter
3. Cl- driven Na+ reabsorption ( via paracellular route)
4. Na+ - K+ pump
13. Na+ can be transported across the luminal
membrane of renal tubular cells by
a) Co-transport with organic solutes
b) Sodium potassium ATPase system
c) Sodium channels
d) Counter transport with H+
e) Counter transport with Ca++
TFTTF
14. Sodium reabsorption occurs
a) 30% in proximal tubule
b) 10% in distal convoluted tubule
c) 60% in loop of henle
d) Aldosterone helps in reabsorption in distal tubule
e) Amiloride mediate reabsorption in collecting ducts
14. Sodium reabsorption occurs
a) 30% in proximal tubule
b) 10% in distal convoluted tubule
c) 60% in loop of henle
d) Aldosterone helps in reabsorption in distal tubule
e) Amiloride mediate reabsorption in collecting ducts
FTFTF
15. The primary function of ascending limb of loop of
Henle of kidney are
a) Active reabsorption of sodium
b) Active reabsorption of chloride
c) Active reabsorption of potassium
d) Passive reabsorption of water
e) Passive reabsorption of urea
15. The primary function of ascending limb of loop of
Henle of kidney are
a) Active reabsorption of sodium
b) Active reabsorption of chloride
c) Active reabsorption of potassium
d) Passive reabsorption of water
e) Passive reabsorption of urea
TTTFF
16. The cells of the distal convoluted tubule
a) reabsorb most of the potassium ions from the glomerular filtrate
b) contain main target cells for ADH
c) form NH4+ ions
d) reabsorb most of the chloride ions from the glomerular filtrate
e) reabsorb potassium ions in exchange for hydrogen ions
16. The cells of the distal convoluted tubule
a) reabsorb most of the potassium ions from the glomerular filtrate
b) contain main target cells for ADH
c) form NH4+ ions
d) reabsorb most of the chloride ions from the glomerular filtrate
e) reabsorb potassium ions in exchange for hydrogen ions
FTFFT
17. Regarding Concentrating ability of urine-
a) Loop of henle- the countercurrent exchanger.
b) Lose in diabetes insipidus.
c) Counter current multiplier creates medullary hyperosmolarity.
d) Impaired with spironolactone use)
e) Impaired with frusemide use)
Medullary interstitial Hyperosmolarity
• At the corticomedullary junction of kidney, interstitial fluid
has osmolarity same as that of plasma which is
300mosm/L
• Medullary interstitial fluid osmolarity increases
progressively with increasing depth into medulla and
attains the value of about 1200mosm/L at the papilla
( deepest medulla). This makes the vertical
corticomedullary interstitial osmotic gradient from 300
mosm/L to 1200 mosm/L
• This medullary interstitial hyperosmolarity is created by
deposition of NaCI and urea into the interstitial space
• NaCI is deposited by countercurrent multiplication
function of LH and urea is deposited by urea trapping
( urea recycling) mechanism
LH as counter current multiplier
• Solutes (NaCI) are actively reabsorbed from the
ascending limb of L and then deeper medulla due
to the counter current flow of filtrate along the
descending and ascending limbs of loop of
Henle.
∙ Urea trapping ( recycling) mechanism

⮚40-60 % of filtered urea is passively reabsorbed from

PCT since PCT is freely permeable to urea. Descending
LH shows limited degree of urea permeability, but
ascending LH, DCT and CD are virtually impermeable to
urea.
⮚Consequently urea gets increasingly concentrated in the
tubule as water is reabsorbed from LH, DCT and CD.
Medullary CD becomes permeable to urea in presence
to ADH. So when filtrate with high urea concentration
reaches the medullary CD, urea diffuses out into the
medullary interstitium to make the space hyperosmolar.
⮚From medullary interstitium the urea again
diffuses into the tubular fluid through descending
LH since the concentration of urea in interstitium
is more than that in descending LH. This diffused
urea again comes out of the tubular fluid into the
interstitium from medullary CD and the process is
repeated again and again.
⮚The consequence of this recycling of urea (exit
from CD and entry into descending LH) helps in
the trapping and accumulation of urea into the
medullary interstitial space.
Medullary interstitial hyperosmolarity created by
countercurrent multiplication of LH and urea
recycling process is preserved (NaC1 and Urea
are not removed) by two mechanisms:
➢ Sluggish blood flow to medulla
Since only 5 % of RBF goes to medulla, the rate of
blood flow to m too slow to wash out deposited
solutes from medullary interstitium.
➢ The countercurrent exchange function of vasa
recta (VR)
Blood enters into the medulla via descending limb of
VR and by U-turn blood exit medulla via ascending
limb of VR. As blood passes down descending limb, it
loses water and gain solutes (NaCl, urea), but when
blood exits medulla through ascending limb, it loses
solutes and gain water. As a result water is removed
from medullary interstitium with persistence of
solutes which make the interstitium hyperosmolar.
17. Regarding Concentrating ability of urine-
a) Loop of henle- the countercurrent exchanger.
b) Lose in diabetes insipidus.
c) Counter current multiplier creates medullary hyperosmolarity.
d) Impaired with spironolactone use)
e) Impaired with frusemide use)
FTTTFT
18. Renal medullary hyperosmolarity is created by
a) Active transport of Na+ from thick segment of ascending limb of
loop of henle
b) Active transport of glucose from proximal convoluted tubule
BVENCE to co
c) Passive diffusion of urea from inner medullary collecting duct
d) Active transport of Nat from collecting duct
e) Active transport of HCO3 from descending limb of loop of henle
18. Renal medullary hyperosmolarity is created by
a) Active transport of Na+ from thick segment of ascending limb of
loop of henle
b) Active transport of glucose from proximal convoluted tubule
BVENCE to co
c) Passive diffusion of urea from inner medullary collecting duct
d) Active transport of Nat from collecting duct
e) Active transport of HCO3 from descending limb of loop of henle
TFTFF
19. Kidney can regulate ECF H+ concentration by:
a) reabsorption of H+
b) secretion of H+
c) reabsorption of HCO3-
d) secretion of HCO3-
e) production of new HCO3-
 Mechanism of acidification of urine
 
Proximal acidification (HCO3-) reabsorption mechanism):
 
• It is concerned with the complete reabsorption of filtered HCO3- mainly
from PCT (80-90%) and partly from ascending limb of Henle (ALH)
(10-20%)
• At normal GFR (180L/day) and normal plasma HCO3- concentration
(25 mmol/L), the tubular load of HCO3- is about 4500 mmol/day
(180X25).
• For reabsorption of very HCO3- from filtrate, one H+ is to be secreted
from tubular cell into lumen. Therefore, PCT and ALH together secrete
about 4500 mmol H+ daily to reabsorb filtered HCO3- completely.
• Compete reabsorption of HCO3- causes reduction of the PH of filtrate
from 7.4 to 6.8.
Distal acidification (HCO3- generation mechanism):
 
▪ It is concerned with excretion of non-volatile metabolic acid
accompanied by generation of new HCO3- within the tubular cells
with its addition to blood.
▪ It happens to occur primarily in collecting duct (CD) and partly in
DCT.
▪ A normal adult individual on average produce about 70 mmol non-
volatile acid per day, which is immediately buffered by body buffers
(mainly HCO3- buffer) to incorporate their protons into body water at
the cost of reduction of plasma HCO3- content by 70 mmol.
H+ + HCO3- 🡪 CO2 + H2O
▪ Cells of CD again generate same amount of protons
(70 mmol) and HCO3- (70 mmol) from body water.
HCO3- (70 mmol) is absorbed laterally to blood to
replace the HCO3- lost internally during buffering and
raises the plasma HCO3- content ration back to normal.
H+ (70 mmol) is secreted into the lumen for excretion.
▪ Most of the H+ secreted in the lumen of CD binds with
NH3 and HPO42+ to form NH+4 & H2PO4- and a little
amount remains free. NH+4 & H2PO4- act as acids
because they can donate protons(H+). NH4+, H2PO4- &
free H+ causes further reduction of filtrate from 6.8 to
as low as 4.5.
▪ Thus, alkaline filtrate becomes acidic urine
Buffer systems acting in renal tubules
Buffer system (S) PK Site of
action
Bicarbonate (HCO3-/CO2) 6.1 PCT.DT
Phosphate 6.8 DT,CDs
(HPO42-/H2PO4-)
Ammonia (NH3/NH4+) 9.0 PCT,DT
Acid substances present in urine:
 NH4+, H2PO4- & free H+
 
PH range of urine is 4.5-8.
Limiting PH of urine: 4.5
19. Kidney can regulate ECF H+ concentration by:
a) reabsorption of H+
b) secretion of H+
c) reabsorption of HCO3-
d) secretion of HCO3-
e) production of new HCO3-
FTTFT
20. Acton of Angiotensin II
a) Systemic vasoconstriction
b) Afferent arteriolar vasodilation
c) Inhibits PTH
d) Synthesis of aldosteron
e) Stimulates thirst
20. Acton of Angiotensin II
a) Systemic vasoconstriction
b) Afferent arteriolar vasodilation
c) Inhibits PTH
d) Synthesis of aldosteron
e) Stimulates thirst
TFFTT
21. Atrial natriuretic peptide causes-
a) Increase GFR
b) Decrease renin secretion
c) Enhance secretion of aldosterone
d) Increase ADH secretion
e) Decrease Nacl reabsorption by the collecting duct
Following hormones act on kidney:
1. Aldosterone
2. ADH
3. ANP
4. Angiotensin II
5. Calcitonin
6. Calcitriol
7. Catecholamine
8. Prostaglandin
9. PTH
10. Dopamine
21. Atrial natriuretic peptide causes-
a) Increase GFR
b) Decrease renin secretion
c) Enhance secretion of aldosterone
d) Increase ADH secretion
e) Decrease Nacl reabsorption by the collecting duct
TTFFT
22. Glomerular function test include
a) Water deprivation test
b) Acid load test
c) Creatinine clearance test
d) Calorie deprivation test
e) Specific gravity of urine
22. Glomerular function test include
a) Water deprivation test
b) Acid load test
c) Creatinine clearance test
d) Calorie deprivation test
e) Specific gravity of urine
FFTFF
23. The renal plasma clearance value of a substance
is
a) Inversely related to its urinary concentration
b) Directly related to the rate of urine formation
c) Directly related to its plasma concentration
d) Expressed in units of volume per unit time
e) The volume of urine that contains the amount of the substance
23. The renal plasma clearance value of a substance
is
a) Inversely related to its urinary concentration
b) Directly related to the rate of urine formation
c) Directly related to its plasma concentration
d) Expressed in units of volume per unit time
e) The volume of urine that contains the amount of the substance
FTFTF
24. By routine and microscopic examination (R/M/E)
of urine we can have idea about
a) Diabetes mellitus
b) Nephropathy 110
c) Multiple myeloma Mo
d) Urinary tract infection
e) Genitourinary tuberculosis
24. By routine and microscopic examination (R/M/E)
of urine we can have idea about
a) Diabetes mellitus
b) Nephropathy 110
c) Multiple myeloma Mo
d) Urinary tract infection
e) Genitourinary tuberculosis
TTTTF
25. 0.9% Sodium chloride solution in water is
a) Standard solution
b) Normal solution of sodium chloride
c) Isotonic solution
d) Crystalloid solution
e) Buffer solution
25. 0.9% Sodium chloride solution in water is
a) Standard solution
b) Normal solution of sodium chloride
c) Isotonic solution
d) Crystalloid solution
e) Buffer solution
TTTTF
26. Compared with intracellular fluid, the
extracellular fluid has lower
a) Osmolality
b) Sodium ion concentration
c) Chloride ion concentration
d) Potassium ion concentration
e) Hydrogen ion concentration
Important electrolytes present in ECF & ICF

Constituen ECF (mmol/L) ICF (mmol/L)

ts
Na+ 135-145 10-14
K+ 3.4-5 135-142
Ca2+ 1.2-2.5 0.1-0.2 umol/L
Mg2+ 0.8-1.5 20-30
Cl- 100-108 3-5
HCO3- 24-27 8-10
Differences between ECF & ICF
ECF ICF
Occupies outside the cells Occupies inside the
cells
High content of Na+, Cl-, High content of K+, Mg2+
Ca2+ & PO43-
Glucose content is high Glucose content is less
Protein content is less Protein content is high
Provides ions & nutrients to Provides essential fluid
cell for maintaining cellular media inside the cell for
life chemical reaction
PO2 = 35 mmHg PO2 = 20 mmHg
PCO2 = 46 mmHg PCO2 = 50 mmHg
PH = 7.4 PH = 7.0
26. Compared with intracellular fluid, the
extracellular fluid has lower
a) Osmolality
b) Sodium ion concentration
c) Chloride ion concentration
d) Potassium ion concentration
e) Hydrogen ion concentration
FFFTT
27.In a person deprived of water for 24-hours three is
an increase in
a) plasma rennin activity
b) ADH secretion
c) plasma atrial natriuretic peptide
d) vagal tone
e) Plasma Na+ concentration
Consequence of osmotic disequilibrium
between ICF and ECF: (Consequence of the
disturbance of ECF osmolarity)
1. When ECF OP < ICF OP: (e.g. infusion of
hypotonic solution):
➢ Cellular overhydration due to water entry into the
cells.
➢ Increased intracellular hydrostatic pressure.
➢ Impairment of cellular metabolic activities.
➢ Cerebral edema leading to coma and even death.
2. When ECF OP > ICF OP: (e.g. infusion of hypertonic
solution):
➢ Cellular dehydration due to water loss from the cells.
➢ Impairment of cellular metabolic activities.
➢ K+ efflux from cells leading to hyperkalemia.
➢ Cerebral dehydration leading to coma and even death.
 
* Change of brain water content by 10% leads to death
following cerebral edema or cerebral dehydration.
27.In a person deprived of water for 24-hours three is
an increase in
a) plasma rennin activity
b) ADH secretion
c) plasma atrial natriuretic peptide
d) vagal tone
e) Plasma Na+ concentration
TTFFT
28. Volume overload indirectly act as pressure
controller by
a) increasing secretion of ADH
b) increasing secretion of atrial natnuretic peptide
c) increasing glomerular filtration rate
d) inhibiting release of renin
e) decreasing tubular reabsorption of glucose
28. Volume overload indirectly act as pressure
controller by
a) increasing secretion of ADH
b) increasing secretion of atrial natnuretic peptide
c) increasing glomerular filtration rate
d) inhibiting release of renin
e) decreasing tubular reabsorption of glucose
FTTTF
29. ADH Secretion stimulated by-
a) Increased plasma osmolarity.
b) ANP.
c) Hypervolaemia)
d) Nausea)
e) Decreased circulating volume)
29. ADH Secretion stimulated by-
a) Increased plasma osmolarity.
b) ANP.
c) Hypervolaemia)
d) Nausea)
e) Decreased circulating volume)
TFFTT
30. Type 1 renal tubular acidosis is characterized by
a) Low sodium
b) Hypercalcemia
c) High serum potassium
d) Failure of H+ ion secretion
e) Normal anion gap.
30. Type 1 renal tubular acidosis is characterized by
a) Low sodium
b) Hypercalcemia
c) High serum potassium
d) Failure of H+ ion secretion
e) Normal anion gap.
FFFTT
31. High anion gap metabolic acidosis occurs in
a) Diabetic ketoacidosis
b) Renal tubular acidosis
c) Diarrhea
d) Vomiting
e) Renal failure
 Causes of Metabolic acidosis:
Disorder Mechanism
A. Normal Anion Gap
∙ Inorganic acid Therapeutic infusion or poisoning with of NH4Cl,
addition HCL
∙ Gastrointestinal base Loss of HCO3 in diarrhea, small bowel fistula,
loss urinary diversion procedure
∙ Renal tubular Urinary loss of HCO3 in proximal RTA
acidosis (RTA) Impaired tubular acid secretion in distal RTA
A. Increased Anion Gap
∙ Endogenous acid Accumulation of ketones with hyperglycemia
load
∙ Diabetic ketoacidosis
∙ Starvation ketosis Accumulation of ketones without hyperglycemia
∙ Lactic acidosis Tissue hypoxia (e.g. shock) or liver disease.
∙ Renal failure Accumulation of organic acids
∙ Exogenous acid load
∙ Aspirin poisoning Accumulation of salicylate
∙ Methanol poisoning Accumulation of salicylate
∙ Ethylene glycol Accumulation of glycolate, oxalate.
31. High anion gap metabolic acidosis occurs in
a) Diabetic ketoacidosis
b) Renal tubular acidosis
c) Diarrhea
d) Vomiting
e) Renal failure
TFFFT
32. Hyperchloremic metabolic acidosis occurs in
a) Renal tubular acidosis
b) Diabetic ketoacidosis
c) Diarrhoea
d) Lactic acidosis
e) Renal failure
32. Hyperchloremic metabolic acidosis occurs in
a) Renal tubular acidosis
b) Diabetic ketoacidosis
c) Diarrhoea
d) Lactic acidosis
e) Renal failure
TFTFF
33. Alkalosis results from
a) persisting vomiting
b) alcoholism
c) Cushing's syndrome
d) hyperaldosteronism
e) Conn's syndrome
33. Alkalosis results from
a) persisting vomiting
b) alcoholism
c) Cushing's syndrome
d) hyperaldosteronism
e) Conn's syndrome
TFTTT
34. Causes of HypovolaemicHypernatraemia
a) Excessive sweating
b) Colonic diarrhoea
c) Hyperosmolar hyperglycaemic state
d) Diabetes insipidus
e) Mannitol infusion
34. Causes of HypovolaemicHypernatraemia
a) Excessive sweating
b) Colonic diarrhoea
c) Hyperosmolar hyperglycaemic state
d) Diabetes insipidus
e) Mannitol infusion
TTTFT
35.Feature of hypotonic hypervolemia-
a) Osmolarity of gained fluid is less than 300mosm/L
b) Na+ concentration of gained fluid is less than that of plasma
c) Both ECF and ICF volume decrease
d) Osmolality ofboth ECF & ICF increase
e) Usually associated with odema
 
 Hypotonic hypervolemia : Clinically common
Features:
⮚Occur following hypotonic fluid gain (osmolarity of
gained fluid is less than 300 mosm/L).
⮚Na+ concentration of gained fluid is less than that of
plasma.
⮚Body total Na+ content increases but plasma Na+ conc.
usually low
⮚Both ECF and ICF volume increase: ECF increases due
to fluid gain and ICF increases due to osmotic gain of
water into cells.
⮚Osmolarity (OP) in both ICF & ECF decreases and
usually associated with edema.
Common causes:
⮚Congestive cardiac failure (CCF) & Nephrotic
syndrome.
⮚Cirrhosis of liver, hepatic failure & Kwashiorkor.
⮚Protein losing enteropathies.
35.Feature of hypotonic hypervolemia-
a) Osmolarity of gained fluid is less than 300mosm/L
b) Na+ concentration of gained fluid is less than that of plasma
c) Both ECF and ICF volume decrease
d) Osmolality ofboth ECF & ICF increase
e) Usually associated with odema
TTFFT
36. Hyperkaliemia may cause
a) Decreased systemic vascular resistance
b) Decreased sodium excretion
c) Increased ammonium production
d) Increased renin secretion
e) Increased aldosterone secretion
Consequences: (effects / complications of
hyperkalemia)
1. Cardiac arrhythmia
2. dardiac arrest (in asystole)
3. Tingling and paresthesis
4. Paresis and paralysis
5. Respiratory muscle paralysis
6. Paralytic ileus
 * Hyperkalemia is less common than hypokalemia, but it is
more dangerous and kills the individual without warning
36. Hyperkaliemia may cause
a) Decreased systemic vascular resistance
b) Decreased sodium excretion
c) Increased ammonium production
d) Increased renin secretion
e) Increased aldosterone secretion
TFFFT
37. Intracellular shit of K+ caused by-
a) Metabolic acidosis
b) 2 agonistβ
c) Aldosterone
d) Calcium-gluconate injections
e) NaHCO3 infusion
Factors regulating transmembrane potassium flux

Factor Function Effect on serum K+

Insulin
Aldosterone Influx Hypokalemia
Acute potassium excess
Alkalosis
β-agonist (epinephrine
α-blocker
Glucagon
ECF hyperosmolarity Efflux Hyperkalemia
Acute potassium deficit
Acidosis
α- agonist (norepinephrine)
β- blocker
37. Intracellular shit of K+ caused by-
a) Metabolic acidosis
b) 2 agonistβ
c) Aldosterone
d) Calcium-gluconate injections
e) NaHCO3 infusion
FTTFT
38. In the hypokalemia, ECG shows
a) Prolonged PR interval
b) ST depression
c) Prolonged QT interval
d) Prominent U wave
e) Tall and slender T wave
ECG changes in electrolytes abnormality:
 
A low K+ level (hypokalaemia) causes:
- Flattening of T wave
- Prolongation of QT interval
- Appearance of U wave on the end of the T wave
 A high K+ level (hyperkalaemia) Causes:
- Tall, wide, peaked (tent like) T wave
- PR interval and QRS complexes are lengthened
- Disappearance of the ST segment

A low plasma Ca++ level (hypercalcaemia) causes:

- Prolongation of the QT interval
 
A high plasma Ca++ level (hypercalcaemia) causes:
- Shortening of the QT interval
The effects of abnormal Mg++ levels are similar to that of
abnormal K+ levels
38. In the hypokalemia, ECG shows
a) Prolonged PR interval
b) ST depression
c) Prolonged QT interval
d) Prominent U wave
e) Tall and slender T wave
TTTTF
39. Following tumour cause hypercalcemia-
a) Bronchial carcinoma
b) Renal cell carcinoma
c) Astrocytoma
d) Multiple myeloma
e) Thyroid carcinoma
Causes of hypercalcaemia
39. Following tumour cause hypercalcemia-
a) Bronchial carcinoma
b) Renal cell carcinoma
c) Astrocytoma
d) Multiple myeloma
e) Thyroid carcinoma
TTFTT ( usually paired organ tumour)
40. Causes of low ionized calcium level in blood-
a) Vit-D deficienay
b) Hypoalbminaemia
c) Thyrotoxicosis
d) Milk-alkali syndrome
e) Metabolic alkalosis
 Hypocalcaemia
 
Hypocalcemia: Adjusted total calcium < 8.4 mg% or 2.1
mmol/L
Causes hypocalcemia:
1. Hypoparathyroidism
2. Vitamin D deficiency
3. Vitamin D resistance
4. Pseudohypoparathyroidism (tissue resistant to PTH)
5. Chronic renal failure
6. Acute pancreatitis
7. Alkalosis
8. Excessive bone mineralization (hungry bone syndrome)
Complications / effects/consequences of
hypocalcemia:
1. Neuromuscular excitement. e.g. tetany, seizure,
bronchospasm, muscle cramps etc.
2. Cardiac irritability, cardiac arrhythmia,
bradycardia, hypotension etc.
3. Psychiatric disturbances
40. Causes of low ionized calcium level in blood-
a) Vit-D deficienay
b) Hypoalbminaemia
c) Thyrotoxicosis
d) Milk-alkali syndrome
e) Metabolic alkalosis
TFFFT