Hemodynamic Disorders+water,electrolyte,acid-base Disorders.

1. What is the mechanism behind swelling of the arm in a patient who has undergone radical mastectomy?

Impaired nerve function causing reduced sensation in the arm

Infection in the surgical site leading to inflammation

*Patient has Lymphedema*Remember that Lymph nodes remove excess fluid and proteins from interstitium(Part of ECF which also includes IntraVascular compartment, but lymphatics remove fluid and protein that leaked from INTRAvascular compartment into Extravascular compartment=Interstitial fluid), surgery most likely damaged lymphatic return>Accumulation of this fluid and protein >Lymphedema of arm.

Surgical complications related to blood clot formation

Lymphedema is the swelling of the arm due to damage to the lymphatic system during surgery, causing accumulation of fluid and proteins. Surgical complications related to blood clots, infection, or nerve dysfunction typically present with different symptoms or consequences.

Explanation

Lymphedema is the swelling of the arm due to damage to the lymphatic system during surgery, causing accumulation of fluid and proteins. Surgical complications related to blood clots, infection, or nerve dysfunction typically present with different symptoms or consequences.

2. CHF will lead to marked edema of which region in bedridden patient?

Head and neck

*Sacrum Not lower extremities(Would be the case in a standing patient)*Remember Edema is caused by movement of Fluid from Intravascular>Extravascular space(Both are part of ECF)-in this case manily trough Increased Hydrostatic pressure(Promotes movement out of the vasculature)

Abdomen

Lower extremities

Edema in bedridden patients with CHF mainly occurs in the sacrum due to increased hydrostatic pressure promoting movement of fluid from the intravascular to the extravascular space.

Explanation

Edema in bedridden patients with CHF mainly occurs in the sacrum due to increased hydrostatic pressure promoting movement of fluid from the intravascular to the extravascular space.

3. Patient has HF/RF what can you say about their oncotic pressure?

Oncotic pressure is increased due to hypoalbuminemia in HF/RF patients

Oncotic pressure remains unaffected in patients with HF/RF

Oncotic pressure is increased due to Na and Water retention in HF/RF patients

*Oncotic pressure is decreased due to Na and Water retention(Renal failure/HF- remember HF can cause renal failure)*Increase in hydrostatic pressure is the mechanism of edema in HF but the point is Oncotic pressure can be decreased too as HF>Renal failure>Na and Water Retention>LESS Oncotic pressure.*Hypoalbuminemia>Decreased oncotic pressure(Less protein) is the major cause of edema in Neprhotic syndrome/Cirrhosis,Malnutrition, but RF can also cause Na and water retention which is another mechanism of Decreased oncotic pressure.*Most common cause of Hypoalbuminebia is Acute/Chronic infection>Decreased oncotic pressure

In patients with HF/RF, oncotic pressure is decreased due to Na and water retention caused by renal failure and heart failure. This leads to decreased oncotic pressure impacting fluid balance and contributing to edema.

Explanation

In patients with HF/RF, oncotic pressure is decreased due to Na and water retention caused by renal failure and heart failure. This leads to decreased oncotic pressure impacting fluid balance and contributing to edema.

4. What causes the *Peau'd orange (Pitted, dimpled appearance of breast) appearance of breast due to carcinoma?

Inflammation of the mammary glands

Hormonal imbalance leading to fluid retention in breast tissue

Invasion of muscle tissue by cancer cells

*Spread of cancer to Dermal Lymphatics, So the mechanism is Lymphatic Obstruction.

5. Why do thiazide diuretics help with Nephrotic syndrome-induced edema?

Because thiazides inhibit renal blood flow, causing a decrease in edema formation.

Because thiazides directly increase intravascular volume, leading to reduced edema.

Because thiazides block the action of aldosterone, resulting in increased fluid retention and exacerbation of edema.

*Because in Nephrotic syndrome your fludid will leak from Intravascular space to Extravascular space(Due to Decreased Oncotic pressure), Less fluid in intravascular space means less blood reaches kidney>Upregulation of RAAS>Na/water retention>More Edema.*Thiazides they promote excretion of Na at distall convoluted tubule by Blocking Na/Cl Symporter(Doesn't need ATP)>Less Na retention>less Fluid will follow+Less decrease in Oncotic pressure> Less edema.

Thiazide diuretics work by promoting Na excretion at the distal convoluted tubule leading to less Na retention and less fluid accumulation in the extracellular space, ultimately helping to reduce edema in patients with Nephrotic syndrome.

Explanation

Thiazide diuretics work by promoting Na excretion at the distal convoluted tubule leading to less Na retention and less fluid accumulation in the extracellular space, ultimately helping to reduce edema in patients with Nephrotic syndrome.

6. What condition can cause pitting edema?

Malnutrition

Dehydration

Allergic reaction

*Increased Hydrostatic pressure(HF.Na retention in interstitial space=part of ECF)*Decreased oncotic pressue(From hypoalbuminemia, Nephrotic syndorme,cirrhosis)*NON-pitting can be caused by lymphedema(Due to Lympathic outfow obstruction),Elephantiasis(due to Wuchera Bancrofti) ,HYPOTHYROIDISM(Pretibial Myxedema-No eating up of GAG's by Thyroid hormone),Graves disease(Pretibial myxedeba due to dysregulation of dermal fibroblasts-which have receptors for TSH Stimulating antibodies.)

Pitting edema is caused by a variety of factors such as increased hydrostatic pressure and decreased oncotic pressure, which can lead to fluid accumulation in the interstitial space. Malnutrition, dehydration, and allergic reactions are not known causes of pitting edema.

Explanation

Pitting edema is caused by a variety of factors such as increased hydrostatic pressure and decreased oncotic pressure, which can lead to fluid accumulation in the interstitial space. Malnutrition, dehydration, and allergic reactions are not known causes of pitting edema.

7. How can a patient with Right HF end up with dyspnea, pulmonary infiltrates, and frothy sputum without fever?

The patient may have an allergic reaction causing respiratory distress.

*Well he can't directly BUT*RHF can cause LHF due to backflow of blood into systemic circulation from right atrium as right ventricle can't pump blood out properly(Patient can develop Nutmeg liver due to blood backing up into SVC/IVC/Hetapic vein/Central vein-look for AST/ALT elevation as it can indicate centrilobular necrosis).*As there is higher workload on left heart it can hypertrophy and fail>Backup of blood into Pulmonary veins(bring oxygenated blood into LA)>RBC leak out into alveoli where macrophages eat them up>Heart failure cells which can produce Frothy sputum when coughed up, don't confuse this with Rusty colored sputum which would make you think about bacterial pneumonia like Strep.pneumo)*Hey don't confuse HF cells(Macrophages filled with hemosiderin-byproduct of hemoglobin from RBC) which is Formed in CHRONIC HF with Transudate that is formed with ACUTE HF (Like few days after MI if patient developes HF,you are more likely to see Transudate=HYpocellular,low protein in Alveoli)

The patient's liver may be failing, leading to pulmonary symptoms.

The patient may have developed a bacterial pneumonia causing the symptoms.

The correct answer explains the pathophysiology behind how Right HF can lead to symptoms without fever, emphasizing the development of Left HF and consequent effects on the pulmonary circulation.

Explanation

The correct answer explains the pathophysiology behind how Right HF can lead to symptoms without fever, emphasizing the development of Left HF and consequent effects on the pulmonary circulation.

8. Which type of fluid collection is likely to be experienced by an elderly man who falls and hits his head in the shower resulting in a crescent-shaped collection in the subdural space?

Cyst-Abnormal sac containing fluid, semi-solid material, or gas.

Abscess-Localized collection of pus within tissues resulting from an infection.

*Hematoma-Collection of blood in potential space/tissue, Most likely subdural because he is old, so what? well Old people/alcoholics and people with Alzheimer's have increased risk of SUBDURAL hematoma because between dura and arachnoid(Subarachnoid space) there is increased Subdural space(due to brain shrinkage) in these conditions>Larger distance bridging veins have to to bridge.*NOTE: BABIES are susceptible to subdural hematoma for different reason-THINNER WALLED BRIDGING veins can be ruptured by SHAKING BABY, also think of abuse.*Now EPIdural hematoma's are common after accidental injuries, Motorcycle accidens, Epidural hematoma LOVES PTERION(Temporal region) where it can damage MIDDLE MENINGIAL ARTERY(Branch of maxillary) but on CT it has LENS Shape.*Note Unlike epidural hematoma, subdural can Cross suture-lines.Now our old playa can have another less severe fluid collection which is called ecchymoses which are often result of Contusion, bruises and basically are blotchy hemorrhage into SKIN(in our case),Mucosal and serosal surfaces(Don't confuse Ecchymoses with Petachiae or purpura, petechiae(Small pinpoint spots on epicardium for ex.) is smaller than 2mm while purpura(In TTP)is larger than 3mm,ecchymoses is the largest one 1-2cm)can be due to trauma. -pEtEchiAE is smAllEst, loves Epicardium.

Edema-Excessive accumulation of fluid in the interstitial spaces, causing swelling.

9. How is the propagation of thrombus from local areas inhibited?

*By Secretions from INTACT endothelium nearby.*PGI2(Prostacyclin) and NO prevent platelet aggregation near intact endothelium by vasodilation and thus prevent propagation of thrombus from damaged to intact sites+ Thrombomodulin present on INTACT endothelium binds up Thrombin and inhibits Clot formation by activating protein C(Anticoagulant factor which along with protein S is inactivated by warfarin and thus INITIALLY you are actually HYPERcoagulable when on warfarin till old factors 2,7,9,10are cleared out)

B. By promoting vasodilation at damaged endothelium sites.

D. By activating protein C to enhance clot formation.

A. By increasing platelet aggregation at intact endothelium sites.

C. By inhibiting the production of PGI2 and NO near intact endothelium.

The correct answer explains how intact endothelium plays a crucial role in inhibiting the propagation of thrombus. Options a, b, and d are incorrect as they do not align with the mechanism described in the correct answer.

Explanation

The correct answer explains how intact endothelium plays a crucial role in inhibiting the propagation of thrombus. Options a, b, and d are incorrect as they do not align with the mechanism described in the correct answer.

10. What is a manifestation of VWF deficiency (Autosomal Dominant) due to a problem with Platelet adhesion?

*Increased bleeding time(defective platelet plug formation)*vWF normally stabilizes Factor 8 by protecting it from proteolysis, factor 8 is involved in Intrinsic coagulation pathway>Defect in intrisnic coagulation pathway>Increased PTT only Not PT.*NOTE:Platelet count is Normal UNLIKE TTP where it is decreased, in vwf def. platelet plug formation is defevtive but platelet count cold be perfectly normal.*Treat with DDAVP>Synthethic analog of vasopressin>INdirect release of vWF from endothelium.

Normal bleeding time (no effect on platelet plug formation)

Increased clotting time (excessive platelet plug formation)

Decreased bleeding time (enhanced platelet plug formation)

VWF deficiency leads to defective platelet plug formation, resulting in an increased bleeding time due to the inability of platelets to stick together properly.

Explanation

VWF deficiency leads to defective platelet plug formation, resulting in an increased bleeding time due to the inability of platelets to stick together properly.

11. What substance, obtained from dense granules of platelets from normal people, induces platelet aggregation in unaffected individuals but does not result in platelet aggregation when added to blood from patients with a bleeding disorder?

Fibrinogen

*Substance that was derived from Dense granules and induces platelet aggregation in unaffected individuals is ADP.*Platelet stimulation By ADP results in exposure of Gp2b/3a on platelets where Fibrinogen can bind up platelets and promote their aggregation, patients could have had Glanzmann Thrombasthenia which is AR or Autoimmune mediated defect in Gp2B/3A receptos> platelet aggregation is defective>Increased bleeding time with normal platelet count, so in our case there is defect in platelet to platelet adhesion due to defect of Gp2B3A(Don't confuse this with AR defect of Gp1B on platelets which in that case can't bind up vWF on endothelium>Increase bleeding time,No platelet agglutination with risonectin.)

Thromboxane A2

Von Willebrand Factor

Substance derived from dense granules that induces platelet aggregation in unaffected individuals is ADP. Platelet stimulation by ADP results in exposure of Gp2b/3a on platelets where Fibrinogen can bind up platelets and promote their aggregation. Patients experiencing this could have Glanzmann Thrombasthenia, a defect in Gp2B/3A receptors affecting platelet aggregation.

Explanation

Substance derived from dense granules that induces platelet aggregation in unaffected individuals is ADP. Platelet stimulation by ADP results in exposure of Gp2b/3a on platelets where Fibrinogen can bind up platelets and promote their aggregation. Patients experiencing this could have Glanzmann Thrombasthenia, a defect in Gp2B/3A receptors affecting platelet aggregation.

12. What is the mechanism of the disease in a young boy with a history of upper airway obstruction due to neck hematoma, decreased Factor 8 activity, normal Platelet Count, increased PTT, and decreased motion in knees and ankles?

Excessive production of thrombin

Increased Platelet Count

*Decrease in production of thrombin.*Decreased factor 8 was complete giveaway, as Factor 8 along with Factor 3 and 5 are Cofactors for catalyzing the reaction that forms Thrombin.*Out patient likely has Hemophilia A.*Note factor 8 is also needed for conversion of factor 10>10a.*Also if you didn't know thrombin(2a) converts fibrinogen to fibrin(Ia)which witht he help of Ca(4) and 13a>Mesh formation that stabilizes platelet plug.*remember Hemophilia A is X linked recessive(Mainly found in boys)

Decrease in production of Factor 8

The correct answer is 'Decrease in production of thrombin'. Factor 8 is necessary for catalyzing the reaction that forms Thrombin, which plays a critical role in converting fibrinogen to fibrin and stabilizing platelet plug. Hemophilia A, characterized by a decrease in Factor 8 activity, is an X-linked recessive disorder primarily found in boys.

Explanation

The correct answer is 'Decrease in production of thrombin'. Factor 8 is necessary for catalyzing the reaction that forms Thrombin, which plays a critical role in converting fibrinogen to fibrin and stabilizing platelet plug. Hemophilia A, characterized by a decrease in Factor 8 activity, is an X-linked recessive disorder primarily found in boys.

13. How would you differentiate Liver parenchymal disease from Antiphospholipid syndrome by transfusion of plasma into the patient?

*Elevated prothrombin(PT) time will be corrected with plasma transfusion from unaffected individual because Liver parenchymal disease(Cirrhosis) can lead to Factor 2,7,9,10 deficiency, because these factors are synthesized in Liver >affecting extrinsic coagulation pathway.(When patient lacks these factors plasma from donor who has these factors will correct elevated prothrombin time due to compensation of these factors by donor plasma but this effects aren't long lasting of course- exact same thing would happen with Warfarin(Leading to vit.k def) or Vit.K def. from other reasons (Like Broad spectrum antibiotics killing your K synthesizing bacteria in gut) BUT Antiphospholipid syndrome involves antibodies that have inhibitory affect on in vitro coagulation tests and is NOT corrected with normal plasma)*Note Antiphospholipid antibodies also prolong PT

Plasma transfusion from unaffected individual will correct elevated prothrombin time in both conditions

Liver parenchymal disease and Antiphospholipid syndrome both show improvement in prothrombin time with plasma transfusion

Plasma transfusion from affected individual will correct elevated prothrombin time in both conditions

14. What is the most common cause of Coronary artery thrombosis in an immobile diabetic patient with Thrombosis of LAD (Branch of LCA)?

Hyperthyroidism

Obesity

*Damage to endothelium as most common cause of Coronary artery thrombosis(N1 killer) is Atherosclerosis(which is accelerated by Diabetes type 1 AND 2)*Stasis of blood flow(Due to prolonged immobilization) is important in Low pressure system-VEINS(Which can embolize from DV of legs most commonly below the knee to Pulmonary arteries>Wedge shaped infarct(Dichotomous branchin) of lungs>Electromechanical dissociation with Acute cor pulmonale>SUDDEN DEATH)

Hypertension

Atherosclerosis is accelerated by Diabetes type 1 AND 2, leading to damage to the endothelium and eventual thrombosis of the coronary artery.

Explanation

Atherosclerosis is accelerated by Diabetes type 1 AND 2, leading to damage to the endothelium and eventual thrombosis of the coronary artery.

15. A young patient with a history of multiple DVTs is most likely to have which cause of hypercoagulable state?

Factor 3 deficiency

*Well what if they describe YOUNG(Teens-early 20's)with history of DVT's and ask you what is MOST likely cause of her hypercoagulable state and yes they will drop factor3,protein C def as distractors ALONG with Homocystinuria(Promotes atherosclerosis>Thrombosis),Smoking,Oral contraceptive use(higher risk i Older patients)*Factor V(Leiden) is best choice, because MULTIPLE DVT's at such a young age most likely indicates inherited coagulopathy from which Facor V def is most common cause of hypercoagulable state.(More than 50% of patient with recurrent DVT's have this mutation)*Remember cause of Factor V deficiency is point mutation(Glutamine Replaces Arginine)>Resistant Factor 5 to Protein C which would normally degrade it.

Protein C deficiency

Homocystinuria

Factor V(Leiden) is the most common cause of hypercoagulable state in patients with recurrent DVTs, especially in young individuals.

Explanation

Factor V(Leiden) is the most common cause of hypercoagulable state in patients with recurrent DVTs, especially in young individuals.

16. A guy with a fracture of his left femoral trochanter is hospitalized and on the 15th day of his hospital stay he develops swelling of the leg, especially below the knee. What is the most likely cause of his death?

B. Fat Embolism Syndrome

D. Idiopathic Thrombophlebitis

A.PULMONARY THROMBOEMBOLISM due to Stasis of Blood flow in venous system>DVT>PE(Remember he was hospitalized for 15 days>Venous stasis)*Fat Embolisms is possibility after fractures but Don't get all wet if you see fracture, Fat Embolism leading to Pulmonary complication would most likely present in FIRST few days(1-3 days)*They can refer to venous thrombosis by name of Phlebothrombosis(Inflammation is not must to use this term)*Don't write Phlebotrhombosis if you see patient with adenocarcinoma of the pacnreas>Trosseau's sign(Migratory thrombophlebitis) if they describe Thrombus on Heart valve or Cardiac Mural endocaridum as that thrombi is example of VEGETATION not phlebotrhombosis.

C. Cardiac Mural endocardium thrombosis

The correct answer is A.Pulmonary Thromboembolism due to Stasis of Blood flow in venous system leading to DVT and PE. Fat Embolism Syndrome is a possibility after fractures but is more likely to present in the first few days. Cardiac Mural endocardium thrombosis and Idiopathic Thrombophlebitis are not the likely causes in this scenario.

Explanation

The correct answer is A.Pulmonary Thromboembolism due to Stasis of Blood flow in venous system leading to DVT and PE. Fat Embolism Syndrome is a possibility after fractures but is more likely to present in the first few days. Cardiac Mural endocardium thrombosis and Idiopathic Thrombophlebitis are not the likely causes in this scenario.

17. What type of thrombus is characterized by fibroblast proliferation and ingrowth of capillaries?

Red thrombus

*Organizing thrombus.*You should be able to recognize this type of thrombus on the picture.

Platelet-rich thrombus

White thrombus

An organizing thrombus is characterized by fibroblast proliferation and ingrowth of capillaries, making it distinct from other types of thrombi.

Explanation

An organizing thrombus is characterized by fibroblast proliferation and ingrowth of capillaries, making it distinct from other types of thrombi.

18. In the context of patent foramen ovale, what type of embolism can occur?

Pulmonary when a left sided thrombus crosses it from left ventricle to pulmonary circulation.

Non-paradoxical when a right sided thrombus remains in the right atria.

*paradoxical when a right sided thrombus crosses it from Right atria to left atria and from there left ventricle>Systemic circulation.*normally right sided thrombus would embolize to lungs while left sided one to systemic ciruclation(Spleen,kidney,brain)

Systemic when a left sided thrombus crosses it from left atria to right atria.

In the presence of a patent foramen ovale, a right sided thrombus can paradoxically embolize to the systemic circulation as described in the correct answer. The incorrect answers do not accurately describe the potential outcomes associated with a patent foramen ovale.

Explanation

In the presence of a patent foramen ovale, a right sided thrombus can paradoxically embolize to the systemic circulation as described in the correct answer. The incorrect answers do not accurately describe the potential outcomes associated with a patent foramen ovale.

19. How does amniotic fluid cause emboli formation and death of a female who has given birth?

From amniotic fluid entering the lungs during childbirth.

*Trough ruptured UTERINE VEINS trough ruptured fetal membranes.*Note if she survives acute phase of Cyanosis followed by shock she still can die from DIC and RDS, if she managed to survive she is at high risk of neurologic defects as long-term complication.

As a result of amniotic fluid entering the bloodstream through the placenta.

Due to excessive intake of amniotic fluid during labor.

Amniotic fluid can cause emboli formation and death of a female who has given birth primarily through ruptured uterine veins and ruptured fetal membranes. If not managed properly, this can lead to serious complications such as DIC, RDS, and long-term neurologic defects.

Explanation

Amniotic fluid can cause emboli formation and death of a female who has given birth primarily through ruptured uterine veins and ruptured fetal membranes. If not managed properly, this can lead to serious complications such as DIC, RDS, and long-term neurologic defects.

20. What characteristic findings would be seen when a medium-sized thromboembolus lodges in a peripheral pulmonary artery branch?

Ischemic necrosis of the lung tissue

*Hemorrhagic infarct of the lung that extends to pleura.Why hemorrhagic? Because Lung has dual supply(Bronchial arteries from SYSTEMIC circulation and Pulmonary arteries)When there is infarct Bronchial arteries can still supply interstitium in the affected area>So red infarct.

Atelectasis of the affected lung lobe

Clear fluid accumulation in the pleural space

The correct answer describes the specific pathophysiological process that occurs when a thromboembolus lodges in a pulmonary artery branch, leading to a hemorrhagic infarct. The incorrect answers do not accurately reflect the characteristic findings associated with this scenario.

Explanation

The correct answer describes the specific pathophysiological process that occurs when a thromboembolus lodges in a pulmonary artery branch, leading to a hemorrhagic infarct. The incorrect answers do not accurately reflect the characteristic findings associated with this scenario.

21. Why does infarct of parenchymal organs result in wedge-shaped infarct?

Because of abundant collateral circulation

*Due to minimal collateral circulation*For ex: Spleen,kidney,Lungs can exhibit wedge-shaped infarcts. however in spleen and kidney you will have Pale infarct due to 1 arterial supply while In the case of lungs we have hemorrhagic infarct(Red) due to dual supply(Bronchial arteries from systemic circulation and Pulmonary arteries)

Due to excess blood flow in the affected area

As a result of compromised lymphatic drainage

Infarcts in parenchymal organs tend to be wedge-shaped due to the limited collateral circulation in these areas.

Explanation

Infarcts in parenchymal organs tend to be wedge-shaped due to the limited collateral circulation in these areas.

22. Why would you have elevated lactate levels in septic shock?

*Remember the Most important sign of shock is hypotension>Hypoperfusion>Less oxygen delivered to tissue>More glycolysis to get ATP somehow>More Pyruvate is converted to Lactate.<Marker of IRReversible stage of shock along with Marked metabolic acidosis.

C. Elevated lactate levels in septic shock are a result of increased oxygen delivery to tissues.

A. Elevated lactate levels in septic shock indicate increased blood glucose levels.

B. Elevated lactate levels in septic shock are due to decreased glycolysis.

D. Elevated lactate levels in septic shock indicate a reversible stage of shock.

In septic shock, elevated lactate levels are a result of increased glycolysis to generate ATP due to the hypoperfusion leading to tissue hypoxia. This metabolic shift towards lactate production is a marker of an irreversible stage of shock and is associated with marked metabolic acidosis.

Explanation

In septic shock, elevated lactate levels are a result of increased glycolysis to generate ATP due to the hypoperfusion leading to tissue hypoxia. This metabolic shift towards lactate production is a marker of an irreversible stage of shock and is associated with marked metabolic acidosis.

23. What is the major cation in Interstitial fluid and Vascular compartment?

Ca

Mg

K

*Na Is the Major cation in ECF(Made up of Vascular compartment+Interstitial fluid)*K is major cation in INTECELLULAR FLUID not Interstitial fluid.(Please don't confuse these 2)*Remember if you are 100 kg your ICF is 40 kg while your ECF is 20kg(In other words ICF is 40% while ECF is 20% of your body weight) in total thus Total Body water is 40+20=60% of Body weight.(2/3 of TBW is ICF while 1/3 is ECF and from ECF 2/3 is Interstitial fluid while 1/3 is Vascular compartment)*Note in simple words Interstitial fluid is space between tissue and vessel that brings blood to it.

Na is the major cation in ECF, which includes the Vascular compartment and Interstitial fluid. K is the major cation in intracellular fluid. Ca and Mg are not the major cations in these compartments.

Explanation

Na is the major cation in ECF, which includes the Vascular compartment and Interstitial fluid. K is the major cation in intracellular fluid. Ca and Mg are not the major cations in these compartments.

24. What could you say about Total Body Na of the patient who has Positive Tilt test?

C) Total Body Na is not related to the positive Tilt test in this patient.

B) This patient is unlikely to have any changes in Total Body Na.

*First of all + tilt test means that when patient rises(Stands/sits) from supine(Lying with your back contacting the bed) BP decreases+HR increases(Tachycardia)*Patient likely has decreased Total Body Na(Major cation in the ECF)*They are also likely to have decreased skin turgor+dry mucous membranes on physical examination.

A) Total Body Na is likely to be increased in this patient.

The correct answer explains that a positive Tilt test is associated with decreased Total Body Na, which leads to symptoms like decreased skin turgor and dry mucous membranes.

Explanation

The correct answer explains that a positive Tilt test is associated with decreased Total Body Na, which leads to symptoms like decreased skin turgor and dry mucous membranes.

25. What happens to ICF when you have a Hyperglycemic patient?

ICF moves from high solute concentration to low solute concentration

*ICF contracts(In contrast in Hyponatremia it Expands)*Remember fluid will move from LOW solute concentration to high SOLUTE(Not water) concentration in patient with hyperglycemia/hypernatremia you have increased Posm in ECF(More solute) thus water will follow and Your ICF will contract.*In our case water moved from low solute concentration in ICF to Higher concentration in ECF>ICF contracted,*Remember Glucose and Na are LIMITED to ECF compartment(Impermeant solutes) and if we change their concentration we alter Osmotic gradient(which will determine where water will flow, this is MOSTLY dependent on Na Concentration)

ICF remains unchanged

ICF expands

Severe hyperglycemia can alter the osmolality balance between the extracellular fluid (ECF) and intracellular fluid (ICF), leading to a contraction of ICF. This is due to the movement of water from an area of low solute concentration in the ICF to a higher solute concentration in the ECF, which is driven by the increased osmolality in the ECF caused by elevated levels of impermeant solutes like glucose and sodium.

Explanation

Severe hyperglycemia can alter the osmolality balance between the extracellular fluid (ECF) and intracellular fluid (ICF), leading to a contraction of ICF. This is due to the movement of water from an area of low solute concentration in the ICF to a higher solute concentration in the ECF, which is driven by the increased osmolality in the ECF caused by elevated levels of impermeant solutes like glucose and sodium.

26. Why is dependent pitting edema called dependent and what is the mechanism?

*It can be due to Too much Na containing fluid in INTERSTITIAL space(Major component of ECF)*Edema fluid has Low protein content and thus it will follow law of gravity easier and will move to dependent parts of our body(Sacral area when supine, ankles when standing)+TBNa increase>Increased Hytrostatic pressure*Increased Total Body Na can also cause formation of ascities(Body cavity effusions-in the case of ascities in Peritoneal cavity)

Dependent pitting edema is caused by excessive protein in the interstitial space.

Fluid in dependent pitting edema does not follow gravity and remains evenly distributed throughout the body.

Dependent pitting edema is usually a result of decreased total body sodium levels.

Dependent pitting edema is named 'dependent' because the edema fluid, which has low protein content, follows gravity and accumulates in dependent parts of the body due to increased total body sodium levels and increased hydrostatic pressure. This mechanism causes fluid to accumulate in areas such as the sacral region when lying down or the ankles when standing.

Explanation

Dependent pitting edema is named 'dependent' because the edema fluid, which has low protein content, follows gravity and accumulates in dependent parts of the body due to increased total body sodium levels and increased hydrostatic pressure. This mechanism causes fluid to accumulate in areas such as the sacral region when lying down or the ankles when standing.

27. What is the most common cause of weight gain in a hospitalized patient?

Medication side effects

Decreased physical activity

*Increased TBNa.*So patient is likely to have dependent pitting edema

Excessive fluid intake

Weight gain in a hospitalized patient is often due to fluid retention, leading to edema. Increased TBNa is a common cause of this fluid retention, resulting in dependent pitting edema.

Explanation

Weight gain in a hospitalized patient is often due to fluid retention, leading to edema. Increased TBNa is a common cause of this fluid retention, resulting in dependent pitting edema.

28. What type of alterations in compartments you are likely to see in a patient with cholera, and how would you treat it?

Cholera leads to Respiratory alkalosis by affecting the respiratory rate of the patient, necessitating ventilation therapy for treatment.

Cholera causes Osmotic diarrhea due to an increase in osmotic pressure within the intestines, requiring osmotic agents for treatment.

Cholera results in Hypernatremia with a decreased extracellular fluid volume, requiring diuretics for treatment.

*Remember Cholera can cause Secretory diarrhea by Permanent activation of Gs>Increased cAMP>Phosphorylation of CL channels>release of CL followed by,Na,Water into lumen)*Secretory diarrhea leads to decrease in TBNa and TBW, this leads to CONTRACTION of ECF however this is ISOTONIC NET LOSS of Na and H20 Thus No osmotic gradient is established>NO FLUID SHIFT BETWEEN COMPARTMENTS.*So Yes Cholera toxin>Rice water diarrhea which is type of Secretory diarrhea thus>Can lead to Hypovolemic Normonatremia, thus MAIN priority treatment is Not antibiotics but is REHYDRATION(NORMAL saline can be used for Isotonic loss of fluid, note Normal saline is used to maintain BP when patient lost Significant amount of Na containing fluid which is possible with DIARRHEA,SWEAT(Hypotonic),BLOOD LOSS)so to get 1 liter of Isotonic saline in ECF(Which is what will maintain BP) you have to infuse 3 liters as 2/3 will go to ICF(remember ECF is only1/3 of TBW)*Alternatively 5%albumin can be better choice as you need to Infuse LESS of it because More of it will remain in Vascular Compartment(Part of ECF responsible for maintaining BP)*Lactated ringer can also be used for these purposes and it is preferred to Isotonic Saline because it can be used to Correct metabolic Acidosis caused by Cholera(YES You loose Bicarbonate with secretory diarrhea because there is Cl/HCO3 exchanger in Large intestine as more CL will reach large intestine more Of it will be reabsorbed at the cost of HCO3 secretion into lumen)

Cholera primarily causes Secretory diarrhea, leading to a net isotonic loss of fluid. The mainstay of treatment is rehydration with isotonic fluids to maintain blood pressure and fluid balance within the body.

Explanation

Cholera primarily causes Secretory diarrhea, leading to a net isotonic loss of fluid. The mainstay of treatment is rehydration with isotonic fluids to maintain blood pressure and fluid balance within the body.

29. How will POsm and Serum Na change with infusion of large amount of Normal saline?

*Normal saline is an Isotonic fluid, thus infusion will not alter POsm and Serum Na,but so Net Isotonic gain of Na and H2O will lead to HyperVolemic Normonatremia.*As Osmotic gradient is not altered there is no Fluid Shift between the compartments.*But THink why could patients with Isotonic gain of fluid develop PITTING edema and Body cavity effusions,remember even though it is ISOTONIC you still have GAIN in Na AND H2O so Both TBNA and TBW will increase,and we already know that Excess Na containing FLuid in Interstitial space(space around tissue cells between them and Vessels)>Dependent pitting edema as hydrostatic pressure is increased and oncotic pressure is decreased due to rise in TBNa and TBW.

Both POsm and Serum Na will decrease due to dilution effect of the saline solution.

POsm will decrease while Serum Na will increase due to the presence of added Na in the saline solution.

POsm will increase while Serum Na will decrease due to the excessive volume of fluid entering the body.

The correct answer explains that the infusion of normal saline does not alter POsm and Serum Na significantly due to its isotonic nature, but leads to a net isotonic gain of Na and H2O resulting in hypervolemic normonatremia. The incorrect answers provide common misconceptions about the effects of infusing normal saline on POsm and Serum Na.

Explanation

The correct answer explains that the infusion of normal saline does not alter POsm and Serum Na significantly due to its isotonic nature, but leads to a net isotonic gain of Na and H2O resulting in hypervolemic normonatremia. The incorrect answers provide common misconceptions about the effects of infusing normal saline on POsm and Serum Na.

30. What happens to ICF when there is Hypotonic Disorders?

ICF volume remains unchanged as there is no significant impact on sodium levels.

ICF will expand only in cases of hypervolemic hyponatremia but not in other hypotonic disorders.

ICF will contract due to increased sodium levels in the ECF.

*ICF will expand as Hyponatremia is always there so fluid will move from this low concentration of solute in ECF to higher concentration of solute into ICF.*Examples: Net gain in water(Increased TBW)>Expansion of ECF but over time it will move into ICF to equilibrate as solute concentration became lower in ECF, so Over time ICF will EXPAND(Net gain in water is an example of EUVolemic Hyponatremia)due to SIADH or too much water drinking.(Note NO edema is produced)*Hypotonic gain-when there is gain of H2O and Na but increase in TBW is More than TBNa>Expansion of ECF and ICF due to HYPERvolemic hyponatremia and can be caused by Cirrhosis,Nephrotic syndrome(Decreased Albumin=low oncotic pressure),RHF(Increased Venous hydrostatic pressure) this type of hypotonic gain can result in PITTING edema and Body effusions(like ascities)

In hypotonic disorders, the movement of water from low solute concentration in ECF to higher solute concentration in ICF results in expansion of ICF. This is a common response in hyponatremia where the solute concentration is lower in ECF. It is important to differentiate from hypervolemic and normovolemic hyponatremia, as the volume shift between ECF and ICF varies.

Explanation

In hypotonic disorders, the movement of water from low solute concentration in ECF to higher solute concentration in ICF results in expansion of ICF. This is a common response in hyponatremia where the solute concentration is lower in ECF. It is important to differentiate from hypervolemic and normovolemic hyponatremia, as the volume shift between ECF and ICF varies.