Kidneys and liver/ The Detoxifying Organs of the body 3rd year 2nd semester Flashcards
Where does the PTH have no effect on? What does it do in regards to electrolytes and what counters its effects?
The Thick Ascending Loop of Henle. Active form of Vitamin D which is 1,25 (OH)2D3 also pronounced 1,25-dihydroxy Vitamin D also generically made and named calcitriol
Where is water reabsorbed and where is Na reabsorbed in relation to the kidney
Water is reabsorbed in the Thin Descending Limb but is impermeable to the Thick ascending Loop of Henle
Where is each electrolyte absorbed and secreted in the kidneys?
The kidneys are very fruegal and only spends energy once and that is at the Na/K ATPase on the basolateral side of the tubular cell
Na- is absorbed from the Thick ascending loop of henle
at the Basolateral Border of the Tubular cell
K - From the ATPase which is on the Basolateral side of the tubular cell
Ca- paracellularly due the potassium pushing it away. This calcium reabsorption is independent of the PTH.
Mg- paracellularly due to potassium pushing it away
Cl - follows the K+ and the Na+ but enters the tubular cell from the secondary symporter
How to differentiate in what environment Kidney stones will grow in?
- Oxalate - is the most common and is grown in an acidic environment
- If it has phosphate it refers to kidney stones grown in an alkaline environment
Hint to better remember use alphabetical order meaning acidic comes before alkaline just like oxalate comes before phosphate
Kidney stones are mostly radiopague or radiolucent?
This is True radiopaque, however uric acid stones are radiolucent which is why you would need to use an ultrasound for it
Radio-: This prefix comes from the Latin word “radius,” meaning ray or beam, typically referring to X-rays or other types of radiation in medical contexts
-opaque: This suffix comes from the Latin word “opacus,” meaning dark or shaded, and in this context, it means not allowing light to pass through or impenetrable by X-rays.
Radiopaque: An adjective describing a substance that does not allow X-rays or other forms of radiation to pass through. These substances appear white or light on radiographic images (e.g., bones, certain contrast agents).
-lucent: This suffix comes from the Latin word “lucere,” meaning to shine or be bright. It refers to something that allows light to pass through or is transparent to radiation.
Radiolucent: An adjective describing a substance that allows X-rays or other forms of radiation to pass through. These substances appear dark or black on radiographic images (e.g., air, soft tissues).
In the DCT if potassium is reabsorbed what does normally it lead too and why?
It leads to metabolic alkalosis because the if the Principal Cell is not working than the alpha intercalate cell (which is the second one) it secretes hydrogen.
What ions are mostly reabsorbed in the Early DCT?
Na +, Cl-, and Ca++
does the liver make protein in grown people or is it from the food? How are proteins made in the body
The liver plays a central role in protein production in adults, not directly from the food we eat, but by processing amino acids (the building blocks of protein) that are derived from food. Here’s a breakdown of how it works:
How the Liver Makes Protein:
Amino Acids from Food:
When you consume protein-containing foods (like meat, eggs, dairy, legumes, etc.), your body breaks them down into amino acids during digestion.
These amino acids enter the bloodstream and travel to the liver.
Protein Synthesis in the Liver:
The liver uses these amino acids to synthesize plasma proteins and other important proteins needed for the body’s functions.
Examples of proteins produced by the liver include:
Albumin: Maintains blood volume and pressure, and transports hormones, fatty acids, and drugs.
Clotting Factors: Help the blood clot properly (important for wound healing).
Enzymes: Involved in digestion and other metabolic processes.
C-reactive protein (CRP): Produced during inflammation, used as an indicator in diagnosing conditions like infections or chronic diseases.
oes the Food Provide the Proteins Directly?
No. While food provides the amino acids needed to build proteins, the liver itself synthesizes these proteins. So, proteins in food are broken down into amino acids and then reconstructed into proteins by the liver and other tissues.
Why Is the Liver So Important in Protein Synthesis?
Liver’s Role in Metabolism: The liver also metabolizes other nutrients, like carbohydrates and fats, to regulate energy levels. It processes the by-products of protein breakdown and ensures amino acids are available for protein creation.
Efficiency: The liver can “store” some amino acids and use them as needed, which is why we don’t need to eat protein every single meal to ensure protein production. However, continuous protein intake is important for overall health.
Summary:
The liver makes most of the body’s proteins using the amino acids derived from food, not from the food proteins directly. These proteins are essential for functions like immune response, blood clotting, and nutrient transport.
What is the global prevalence of chronic kidney disease (CKD)?
A) 5-7%
B) 11-13%
C) 20-25%
D) 30-35%
Correct Answer: B) 11-13%
Explanation:
A) 5-7% – Incorrect. The global prevalence is higher than this range.
B) 11-13% – Correct. This is the documented global prevalence of CKD.
C) 20-25% – Incorrect. This overestimates the prevalence of CKD.
D) 30-35% – Incorrect. This is an even greater overestimation of CKD prevalence.
Epidemiology of CKD
* 11 to 13% global prevalence of CKD.
* In the US, there is a 14% prevalence of CKD based on the NHANES 2017-2020.
* In Canada, the prevalence of CKD is 71.9 per 1000 individuals, using data from primary care across five provinces.
* In 2020, over 50,000 Canadians were living with end-stage kidney disease.
Which of the following is NOT a risk factor for CKD?
A) Hypertension
B) Diabetes
C) Proteinuria
D) Appendicitis
Correct Answer: D) Appendicitis
Explanation:
A) Hypertension – Incorrect. Hypertension is a well-known risk factor for CKD.
B) Diabetes – Incorrect. Diabetes is a major contributor to CKD due to its effect on kidney function.
C) Proteinuria – Incorrect. Proteinuria (excess protein in urine) is an indicator and risk factor for CKD.
D) Appendicitis – Correct. Appendicitis is an acute inflammatory condition that does not contribute to CKD.
**CKD Risk Factors **
* Acute Kidney Injury
* Autoinflammatory Diseases (e.g., lupus, vasculitis, cancer immunotherapy)
* Hypertension
* Proteinuria
* Diabetes and Metabolic Syndrome
* Cardiovascular Disease
* Heart Failure
Which of the following statements about nephron loss is FALSE?
A) Aging can contribute to nephron loss.
B) Nephron hypertrophy occurs as compensation for nephron loss.
C) Hypertension and hyperfiltration contribute to nephron loss.
D) Nephron loss is always irreversible.
Correct Answer: D) Nephron loss is always irreversible.
Explanation:
A) Aging can contribute to nephron loss. – True. Aging naturally reduces the number of nephrons.
B) Nephron hypertrophy occurs as compensation for nephron loss. – True. The remaining nephrons enlarge to compensate for the loss.
C) Hypertension and hyperfiltration contribute to nephron loss. – True. These factors increase stress on the kidneys.
D) Nephron loss is always irreversible. – False. In some cases (e.g., acute kidney injury), nephron function can be partially restored.
CKD Pathogenesis
* Nephron Loss
* Aging, kidney injury, surgical loss (nephrectomy for cancer or
kidney donation).
* Nephron hypertrophy
* Hypertension/hyperfiltration
* Impaired glomerular filtration
* Vascular disease, ischemia, glomerular disease
* Fibrosis
* Glomerulosclerosis (hypertension, smoking, dyslipidemia)
* Tubular atrophy, interstitial fibrosis (Decreased filtration
rate)
Which of the following is a common complication of CKD?
A) Hyperkalemia
B) Hypophosphatemia
C) Hypernatremia
D) Alkalosis
Correct Answer: A) Hyperkalemia
Explanation:
A) Hyperkalemia – Correct. Impaired kidney function leads to potassium retention.
B) Hypophosphatemia – Incorrect. CKD is more commonly associated with hyperphosphatemia.
C) Hypernatremia – Incorrect. CKD often leads to sodium retention, but not necessarily hypernatremia.
D) Alkalosis – Incorrect. CKD more commonly leads to metabolic acidosis.
Complications of Chronic Kidney Disease
* Accumulation of nitrogenous waste
Uremia
* Gout
* Pruritis
* Neurological complications, which may include depression, uremic encephalopathy, and uremic polyneuropathy
* Fluid, Electrolyte, and Acid-Base Disorders
Sodium retention (peripheral edema)
Hyperkalemia
Hyperphosphatemia
Metabolic acidosis
Which of the following is a common complication of Chronic Kidney Disease (CKD)?
a) Hypercalcemia
b) Mineral and Bone Disorders (CKD-MBD)
c) Low potassium levels
d) Hyperlipidemia
Answer: b) Mineral and Bone Disorders (CKD-MBD)
Explanation: A) Incorrect due to hypercalcemia not being a typical complication of CKD; instead, phosphate retention and altered Vitamin D metabolism are common.
B) Correct due to CKD causing mineral and bone disorders (CKD-MBD), which include phosphate retention and high PTH levels due to impaired phosphorus excretion and altered Vitamin D metabolism.
C) Incorrect due to CKD typically causing hyperkalemia, not low potassium levels.
D) Incorrect as it does not directly result from CKD but may be a secondary effect in some cases.
Complications of Chronic Kidney Disease
* Mineral and Bone Disorders (CKD-MBD)
Reduced excretion of phosphorus with altered Vitamin D metabolism leads to
High PTH levels
Phosphate retention
* Renal osteodystrophy
Extra-osseous calcification, including arterial, valvular, myocardial and pruritis and joint pain
Which of the following is a goal of nutritional therapy for CKD?
a) Decrease energy intake to limit fat accumulation
b) Control progression of renal osteodystrophy
c) Increase protein intake to avoid malnutrition
d) Increase phosphorus intake to prevent bone loss
Answer: b) Control progression of renal osteodystrophy
B) Correct due to one of the key goals of nutritional therapy being to control the progression of renal osteodystrophy, which includes managing mineral imbalances and bone health.
Explanation: A) Incorrect due to a decrease in energy intake being counterproductive in CKD; adequate energy intake is needed to avoid protein-energy wasting.
C) Incorrect due to protein intake being carefully managed (typically reduced in CKD to prevent kidney damage).
D) Incorrect as it does not align with managing CKD-MBD, where phosphate levels should be controlled, not increased.
What is the most common type of gallstone found in industrialized countries?
a) Pigment stones
b) Cholesterol stones ✅
c) Calcium oxalate stones
d) Uric acid stones
(b) Correct: Cholesterol stones are the most common type in industrialized countries due to dietary factors and metabolic conditions.
(a) Incorrect: Pigment stones are more common in developing countries and are associated with chronic hemolytic conditions and infections.
(c) Incorrect: Calcium oxalate stones are kidney stones, not gallstones.
(d) Incorrect: Uric acid stones are also associated with kidney stone disease, not gallstones.
Further explained
I am guessing cholesterol stones are fat/ lipid stones and not gallbladder stones but because estrogen decreases the release of bile and progesterone slows down the contractions this is how cholestorol stones occur
Cholesterol stones are actually a type of gallstone—they form in the gallbladder, but their primary component is cholesterol rather than pigment or calcium salts.
Here’s how estrogen and progesterone contribute to cholesterol stone formation:
Estrogen increases cholesterol secretion into bile → This makes bile more cholesterol-saturated, increasing the risk of stone formation.
Progesterone slows gallbladder emptying → This leads to stasis (bile sitting in the gallbladder too long), which encourages stone growth.
Together, high cholesterol content + slow bile movement = cholesterol stones.
So, while cholesterol stones are a type of gallstone, they specifically result from an imbalance in cholesterol secretion and gallbladder motility, rather than just excess fat intake alone.
What are pigment stones primarily composed of?
a) Cholesterol monohydrate
b) Bilirubin calcium salts ✅
c) Triglycerides
d) Uric acid
(b) Correct: Pigment stones are composed of bilirubin calcium salts, which form due to excessive bilirubin production or bile infections.
Explanation:
(a) Incorrect: Cholesterol monohydrate is the main component of cholesterol stones, not pigment stones.
(c) Incorrect: Triglycerides are fats and are not involved in gallstone formation.
(d) Incorrect: Uric acid stones are found in the kidneys, not in the gallbladder.
- Are Pigment Stones the Same as Calcium Stones?
Not exactly, but there is some overlap.
Pigment stones are made primarily of unconjugated bilirubin mixed with calcium salts (along with some inorganic components).
Calcium stones (as in kidney stones) are primarily calcium oxalate or calcium phosphate, which are different from pigment stones in the gallbladder.
So, while pigment stones contain calcium, they are not pure calcium stones. Instead, their formation is more linked to excess bilirubin, which binds with calcium to form insoluble stones.
What is the primary precursor for bile synthesis in the liver?
a) Bilirubin
b) Fatty acids
c) Cholesterol ✅
d) Phospholipids
(c) Correct: Bile acids are synthesized from cholesterol in the liver.
Explanation:
(a) Incorrect: Bilirubin is a breakdown product of red blood cells and is excreted in bile, but it is not the precursor for bile synthesis.
(b) Incorrect: Fatty acids are absorbed and transported via bile, but they are not the starting material for bile production.
(d) Incorrect: Phospholipids are a component of bile but are not the main precursor.
Review of Bile formation
* Bile is synthesized from cholesterol in the liver into primary bile acids.
Conjugated into bile salts
prior to secretion
* Primary bile salts
* Other components include:
Water (85-95%), electrolytes, phospholipids, IgA, excretory waste products
Which of the following is NOT a function of bile?
a) Breakdown and absorption of lipids
b) Elimination of waste products like bilirubin
c) Digestion of carbohydrates ✅
d) Maintaining intestinal mucosal integrity
(c) Correct: Bile does not play a direct role in carbohydrate digestion, which is mainly done by amylase.
Explanation:
(a) Incorrect: Bile emulsifies fats, aiding in lipid digestion and absorption.
(b) Incorrect: Bile helps remove waste products like bilirubin and excess cholesterol.
(d) Incorrect: Bile contains immunoglobulins that support intestinal mucosal integrity.
- Purpose of Bile?
Review of Bile excretion
* Bile production by the liver serves 2 functions
Elimination of exogenous and endogenous waste products eg bilirubin and cholesterol
Promotes digestion and absorption of lipids from the intestine
Function of Bile
* Bile salts play a key role in a variety of physiologic and pathophysiologic processes
* Excreted into the small intestine via bile
* Bile has immunoglobulins that support integrity of intestinal mucosa
* Bile responsible for breaking down fats in fatty acids for absorption from the gastrointestinal tract
Where does most bile reabsorption occur?
a) Duodenum
b) Jejunum
c) Terminal ileum ✅
d) Colon
(c) Correct: The terminal ileum actively reabsorbs bile acids and returns them to the liver via enterohepatic circulation.
Explanation:
(a) Incorrect: The duodenum is where bile is released to aid digestion but not significantly reabsorbed.
(b) Incorrect: The jejunum mainly absorbs nutrients, not bile acids.
(d) Incorrect: The colon is where some bile acids may undergo bacterial modification but is not the primary site of reabsorption.
Enterohepatic circulation
* Bile acids undergo enterohepatic circulation
Primarily reabsorbed in the terminal ileum via active transport and travel back to the liver via portal circulation
Colonic bacteria can deconjugate and dehydroxylate bile acids, allowing some passive diffusion
What role do colonic bacteria play in bile metabolism?
a) They deconjugate and dehydroxylate bile acids ✅
b) They completely degrade bile acids into waste
c) They secrete bile acids for digestion
d) They prevent enterohepatic circulation
Explanation:
(a) Correct: Colonic bacteria modify bile acids, which can then be passively reabsorbed.
(b) Incorrect: Bacteria modify bile acids but do not completely degrade them.
(c) Incorrect: The liver synthesizes bile acids, not bacteria.
(d) Incorrect: Bacteria modify bile acids, but enterohepatic circulation still occurs.
What initiates the formation of cholesterol stones?
a) Biliary tract infections
b) Supersaturation of bile with cholesterol ✅
c) Increased bile acid secretion
d) Excessive water loss from bile
(b) Correct: When cholesterol exceeds the solubilizing capacity of bile, it crystallizes and forms stones.
Explanation:
(a) Incorrect: Infections contribute to pigment stones but not cholesterol stones.
(c) Incorrect: Increased bile acid secretion helps prevent gallstones.
(d) Incorrect: Dehydration of bile contributes, but supersaturation is the main cause.
Cholelithiasis
- Cholesterol stones
Cholesterol concentrations exceed the solubilizing capacity of bile (supersaturation) - cholesterol can no longer remain dispersed and nucleates into solid cholesterol monohydrate crystals
- Hypersecretion of mucus in the gallbladder traps the nucleated crystals, leading to their aggregation into stones
- Impaired motility of the gallbladder leads to stasis, allowing progression to macroscopic stones
Which of the following conditions is most associated with pigment stone formation?
a) High cholesterol diet
b) Chronic hemolytic anemia ✅
c) Biliary stasis
d) High-fat meal consumption
(b) Correct: Chronic hemolysis increases bilirubin production, leading to pigment stone formation.
Explanation:
(a) Incorrect: High cholesterol intake is linked to cholesterol stones, not pigment stones.
(c) Incorrect: Biliary stasis promotes cholesterol stones more than pigment stones.
(d) Incorrect: High-fat diets influence cholesterol stone formation.
What is a possible complication of a gallstone blocking the common bile duct?
a) Acute pancreatitis ✅
b) Gastric ulcer
c) Peptic ulcer disease
d) Appendicitis
(a) Correct: A gallstone blocking the common bile duct can also obstruct the pancreatic duct, leading to pancreatitis.
Explanation:
(b) Incorrect: Gallstones do not directly cause gastric ulcers.
(c) Incorrect: Peptic ulcers are caused by H. pylori and NSAIDs, not gallstones.
(d) Incorrect: Appendicitis is unrelated to gallstones.
What long-term complication may arise from chronic cholelithiasis?
a) Secondary biliary cirrhosis ✅
b) Kidney stones
c) Fatty liver disease
d) Diabetes mellitus
(a) Correct: Chronic obstruction of bile flow can cause liver damage, leading to secondary biliary cirrhosis.
Explanation:
(b) Incorrect: Gallstones do not cause kidney stones.
(c) Incorrect: While liver disease may be linked, fatty liver disease is unrelated to gallstones.
(d) Incorrect: Diabetes is a risk factor for gallstones but not a complication.
Cholelithiasis
* Absence of bile in the intestine impairs fat absorption
* If uncorrected, bile can back-up into the liver causing liver damage
Secondary biliary cirrhosis
* Obstruction of the common bile duct can lead to acute pancreatitis if the pancreatic duct gets blocked.
Which of the following is NOT a non-modifiable risk factor for gallstones?
a) Older age
b) Female sex
c) Pregnancy
d) High dietary fat intake ✅
**(d) Correct: Dietary fat intake is modifiable.
**
Explanation:
(a) Incorrect: Age is a non-modifiable risk factor.
(b) Incorrect: Women have a higher risk due to hormonal effects.
(c) Incorrect: Pregnancy increases gallstone risk.
Gallstone Risk Factors
* Non-modifiable risk factors
Female, Pregnancy, Older age, Family history
* Modifiable risk factors:
High dietary fat intake long term
Rapid weight loss
Sedentary lifestyle
Altered gut microflora
Hyperinsulinemia
Obesity/metabolic syndrome/diabetes
Physical inactivity
Certain medications
Parenteral nutrition
Medications – statins, OCPs, estrogen
Which is the correct order of bile flow from the liver to the intestine?
a) Hepatocyte → Bile ductules → Cystic duct → Bile canaliculi → Common bile duct
b) Hepatocyte → Bile canaliculi → Bile ductules → Common hepatic duct → Cystic duct → Common bile duct → Duodenum ✅
c) Hepatocyte → Common bile duct → Cystic duct → Bile canaliculi → Bile ductules
d) Hepatocyte → Duodenum → Common bile duct → Cystic duct → Bile canaliculi
(b) Correct: This follows the correct sequence of bile transport from the liver to the small intestine.
(a, c, d) Incorrect: These have incorrect sequences that do not follow the anatomical flow of bile.
How do oral contraceptive pills (OCPs) contribute to gallstone formation?
a) They increase cholesterol secretion while decreasing bile acids ✅
b) They increase bile acid production and prevent stasis
c) They improve gallbladder motility, reducing the risk of stone formation
d) They decrease cholesterol secretion and increase bile flow
(a) Correct: Estrogen in OCPs increases cholesterol secretion while reducing bile acids, promoting supersaturation.
(b) Incorrect: OCPs reduce bile acids, not increase them.
(c) Incorrect: Progesterone actually slows gallbladder motility, increasing stasis.
(d) Incorrect: The opposite occurs—cholesterol secretion increases while bile acids decrease.
Cholesterol stone formation
OCPs & pregnancy
* Estrogen increases hepatic secretion of cholesterol while
decreasing bile acids.
* Progesterone inhibits discharge of bile from the gallbladder (ie slower emptying) => stasis
Several factors increase biliary cholesterol secretion
* Increasing age, obesity, ethnicity, familial predisposition, diet high in calories & cholesterol, metabolic diseases associated with high serum cholesterol (eg. Diabetes, genetic hyperlipoproteinemias, etc)
Disorders that interfere with enterohepatic circulation of bile acids can also favour gallstone formation
* Pancreatic insufficiency (eg. CF, CD)
What happens to bile composition as it travels from the liver through the bile ducts and gallbladder?
a) It remains unchanged
b) It becomes more dilute
c) It becomes more concentrated ✅
d) It loses its ability to emulsify fats
(c) Correct: Water and electrolytes are reabsorbed, making bile more concentrated.
Explanation:
(a) Incorrect: Bile undergoes modifications along the ducts and gallbladder.
(b) Incorrect: Bile actually becomes more concentrated in the gallbladder.
(d) Incorrect: Bile still retains its function of emulsifying fats.
Which of the following factors is most directly associated with pigment stone formation?
a) Excessive bilirubin production (e.g., chronic hemolytic anemia) ✅
b) Excess dietary cholesterol
c) Hypersecretion of mucus in the gallbladder
d) Increased estrogen levels
(a) Correct: Excessive bilirubin production leads to the accumulation of insoluble calcium bilirubinate salts, which contribute to pigment stone formation.
Explanation:
(b) Incorrect: Dietary cholesterol is more relevant to cholesterol stones, not pigment stones.
(c) Incorrect: Mucus hypersecretion plays a role in cholesterol stone formation, not pigment stones.
(d) Incorrect: Estrogen increases cholesterol secretion, influencing cholesterol stones rather than pigment stones.
What is a major function of bile acids in the digestive system?
a) Emulsification and absorption of dietary fats ✅
b) Neutralization of stomach acid
c) Stimulation of insulin secretion
d) Production of red blood cells
(a) Correct: Bile acids help break down large fat globules into smaller micelles, aiding in fat absorption.
Explanation:
(b) Incorrect: Bile is alkaline, but its primary function is not acid neutralization (which is mainly the role of bicarbonate from the pancreas).
(c) Incorrect: Bile does not stimulate insulin secretion.
(d) Incorrect: Red blood cells are produced in the bone marrow, not the liver or gallbladder.
How are bile acids reabsorbed and recycled in the body?
a) Excreted through urine
b) Reabsorbed in the terminal ileum and returned to the liver via the portal circulation ✅
c) Absorbed in the stomach and re-used for fat digestion
d) Converted into cholesterol in the pancreas
Explanation:
(a) Incorrect: Bile acids are not excreted through urine; they undergo enterohepatic circulation.
(b) Correct: The majority of bile acids are actively transported in the terminal ileum and returned to the liver for reuse.
(c) Incorrect: Bile acids are absorbed in the ileum, not the stomach.
(d) Incorrect: Bile acids do not convert into cholesterol in the pancreas.
What is a potential consequence of gallstone obstruction of the common bile duct?
a) Secondary biliary cirrhosis ✅
b) Increased red blood cell production
c) Decreased stomach acid production
d) Enhanced bile acid reabsorption
(a) Correct: A blocked bile duct can lead to bile backup in the liver, causing liver damage and secondary biliary cirrhosis.
Explanation:
(b) Incorrect: Gallstones do not affect red blood cell production.
(c) Incorrect: Stomach acid production is not related to gallstone obstruction.
(d) Incorrect: If bile flow is obstructed, reabsorption in the ileum is actually reduced.
- Why Is It Called Secondary Biliary Cirrhosis?
The term “secondary” refers to the cause of the cirrhosis.
Primary Biliary Cirrhosis (now called Primary Biliary Cholangitis, PBC) → an autoimmune disease that damages bile ducts inside the liver.
Secondary Biliary Cirrhosis (SBC) → caused by chronic obstruction of bile flow (e.g., due to gallstones, tumors, or strictures).
Why Does This Happen?
A gallstone blocks the common bile duct, preventing bile from flowing out.
Bile backs up into the liver, causing chronic inflammation and damage to liver cells.
Over time, persistent bile accumulation and inflammation lead to fibrosis (scarring), which eventually results in cirrhosis (liver failure due to scarring).
So, it’s called secondary because it is caused by an obstruction (like gallstones), rather than an autoimmune disease like primary biliary cirrhosis.
Which of the following is a modifiable risk factor for cholelithiasis?
a) Female sex
b) Older age
c) Obesity and metabolic syndrome ✅
d) Family history
(c) Correct: Obesity, metabolic syndrome, and diabetes increase biliary cholesterol secretion, making them modifiable risk factors.
Explanation:
(a, b, d) Incorrect: These are non-modifiable risk factors.
Why do oral contraceptives (OCPs) increase the risk of gallstones?
a) They increase bile acid secretion
b) They prevent gallbladder contraction
c) Estrogen increases hepatic cholesterol secretion, while progesterone slows gallbladder motility ✅
d) They increase bile flow
(c) Correct: Estrogen increases cholesterol secretion, while progesterone slows bile release, leading to stasis and gallstone formation.
Explanation:
(a) Incorrect: OCPs decrease bile acids, not increase them.
(b) Incorrect: Progesterone slows gallbladder emptying, but estrogen’s effect is more relevant.
(d) Incorrect: Bile flow actually decreases due to progesterone’s effect.
Which dietary intervention helps reduce gallstone formation?
a) High fiber intake (>25g/day) ✅
b) High refined carbohydrate intake
c) Very low-fat diet
d) Increased saturated fat intake
(a) Correct: High fiber reduces cholesterol saturation in bile, lowering gallstone risk.
Explanation:
(b) Incorrect: Refined carbohydrates increase cholesterol saturation in bile.
(c) Incorrect: Very low-fat diets can worsen stasis by reducing gallbladder contractions.
(d) Incorrect: Saturated fat increases cholesterol secretion, which can contribute to stone formation.
Why is a traditional low-fat diet for cholelithiasis now questioned?
a) Low-fat intake reduces gallbladder contractions, potentially leading to bile stasis and stone formation ✅
b) Low-fat diets increase cholesterol levels
c) Dietary fat has no effect on bile production
d) High-fat diets reduce bile saturation
(a) Correct: Reducing dietary fat intake can actually lead to stasis, as dietary fats stimulate gallbladder contractions.
Explanation:
(b) Incorrect: A low-fat diet does not increase cholesterol levels.
(c) Incorrect: Dietary fat does influence bile production.
(d) Incorrect: High-fat diets can increase cholesterol saturation, not reduce it.
Dietary interventions - Cholelithiasis
* Limit foods triggering pain - Eg. Fried/greasy foods
Traditionally a low-fat diet was recommended as one of the mainstays of cholelithiasis treatment, however recent evidence calls into question its efficacy
* Can anyone suggest two possible rationales for this
recommendation?
1) dietary fats are a potent stimulator of gallbladder contraction, thus
* Lower dietary fats less gallbladder contraction reduced postprandial pain
* What are some concerns with this rationale?
2) Reduced total dietary fat, particularly saturated fat, leads to a reduction in plasma cholesterol
1) Problems with this rationale:
* Gallbladder also contracts spontaneously & in response to intake of mixed meals (thus could still have pain)
* Reduced gallbladder contraction & emptying
stasis increased risk of stone formation
2) Problems with this rationale:
* Evidence is based on old trials modifying dietary cholesterol level (which are not associated with plasma cholesterol levels) and (unsurprisingly) did not demonstrate efficacy.
How can bacterial overgrowth contribute to gallstone formation?
a) Bacteria can deconjugate bile acids, making them ineffective for emulsifying fats ✅
b) Bacteria increase gallbladder motility
c) Bacterial overgrowth prevents cholesterol secretion
d) Bacteria reduce bile production in the liver
Explanation:
(a) Correct: Bacterial deconjugation of bile acids reduces their ability to emulsify fats, contributing to gallstone risk.
(b) Incorrect: Bacterial overgrowth does not increase gallbladder motility.
(c) Incorrect: Bacteria do not prevent cholesterol secretion but instead alter bile composition.
(d) Incorrect: Bacteria affect bile acids, not bile production
What does conjugated and unconjugated mean?
These terms refer to bilirubin, a waste product from the breakdown of red blood cells.
1️⃣ Unconjugated Bilirubin (Indirect Bilirubin)
- Not water-soluble → Cannot be excreted in urine
- Travels in the blood bound to albumin
- Needs to be processed by the liver to become soluble (adds glucuronic acid → becomes conjugated)
2️⃣Conjugated Bilirubin (Direct Bilirubin)
* Water-soluble→ Can be excreted
* The liver adds glucuronic acid to bilirubin in a process called conjugation
* Secreted into bile → excreted into the intestines
In the intestines:
Bacteria convert it into urobilinogen
Some urobilinogen → absorbed back into blood → kidneys → excreted in urine (as urobilin, gives urine its yellow color)
Most urobilinogen → converted to stercobilin → excreted in feces (gives feces its brown color)
Unconjugated bilirubin can build up in conditions like hemolysis or liver failure (since it can’t be excreted easily).
Conjugated bilirubin builds up when there’s bile duct obstruction (since it can’t flow into the intestines).
Why Are They Called “Indirect” and “Direct” Bilirubin?
This comes from how they are measured in lab tests:
Indirect Bilirubin (Unconjugated) → Doesn’t react directly with the reagent used in lab tests, requires a solvent
Direct Bilirubin (Conjugated) → Reacts directly with the reagent, making it easier to measure
💡 Key Takeaways:
Unconjugated (indirect) bilirubin → Cannot be excreted, must be processed by the liver first
Conjugated (direct) bilirubin → Excreted in bile → feces (mostly) and urine (small amount)
High unconjugated bilirubin = Problem with bilirubin processing (e.g., hemolysis, liver dysfunction)
High conjugated bilirubin = Problem with bile excretion (e.g., bile duct obstruction, cholestasis)
Which of the following is a major cause of acute pancreatitis?
A) Low dietary fiber intake
B) Biliary tract obstruction
C) High magnesium intake
D) Low-fat diet
✅ Correct Answer: B) Biliary tract obstruction
👉 Why? A gallstone or sludge blocking the bile duct prevents pancreatic secretions from exiting, leading to enzyme activation inside the pancreas.
❌ Wrong Answers:
A) Low dietary fiber intake: Fiber is important for overall digestion but does not directly cause pancreatitis.
C) High magnesium intake: Magnesium is beneficial for gallbladder health, not a cause of pancreatitis.
D) Low-fat diet: While dietary fats play a role in gallbladder function, they do not directly cause pancreatitis.
Acute pancreatitis common etiologies:
Alcohol ingestion (25-35% of cases):
* Leads to excessive protein in pancreatic secretions, “plugs” the ducts
* Direct toxic effects on acinar cells
* Causes contraction of the sphincter of Oddi
Biliary tract obstruction (40-70% of cases):
* Pancreatic secretions are stuck in the ducts, due to
a gallstone or sludge blocking outflow
Common factor = blockage of ducts
- Other causes
End stage renal disease
Lupus
Biliary tract disease
Abdominal traumas
Dyslipidemias (very high triglycerides
Pancreatic cancer
Pharmaceuticals – many classes can contribute or cause - Antidepressants-
- Antibiotics – tetracycline, rapamycin
- Statins
- Estrogens
- Corticosteroids
- NSAIDS
Which of the following is a key characteristic of acute pancreatitis?
A. It leads to a decrease in serum amylase and lipase levels.
B. Abdominal pain is a hallmark symptom.
C. It is only caused by excessive alcohol consumption.
D. It is treated with antibiotics as the primary intervention.
Correct Answer: B. Abdominal pain is a hallmark symptom.
A: This is incorrect. Acute pancreatitis is characterized by elevated serum amylase and lipase levels, not a decrease.
B: Correct. Abdominal pain is a key symptom of acute pancreatitis, often intense and referred to the back or shoulder.
C: This is incorrect because acute pancreatitis can be caused by a variety of factors, including biliary tract disease, high triglycerides, and pharmaceuticals.
D: This is incorrect. Antibiotics are not the primary treatment for acute pancreatitis; instead, supportive care like fluid resuscitation and enteral nutrition is used.
Acute pancreatitis Clinical features:
Abdominal pain is the cardinal manifestation of acute
pancreatitis
* Constant, intense and often referred to the upper back or
shoulder
* Severity varies (moderate to quite severe)
* Anorexia, nausea, and vomiting frequently accompany the
pain
Systemic effects of severe acute pancreatitis (systemic inflammation, hemorrhage, and fluid loss into abdomen) result in a medical emergency.
- Patients can rapidly proceed to shock and kidney failure
What complication is common in severe acute pancreatitis?
A. Renal failure
B. Hypotension
C. Chronic liver disease
D. Acute respiratory distress syndrome (ARDS)
Correct Answer: D. Acute respiratory distress syndrome (ARDS)
D: Correct. ARDS is a severe, life-threatening complication of acute pancreatitis, often due to systemic inflammation.
A: This is incorrect. While renal failure can occur in severe cases, ARDS is a more common complication of acute pancreatitis.
B: This is incorrect. Hypotension can result from severe pancreatitis, but ARDS is more commonly associated with it.
C: This is incorrect. Chronic liver disease is not a primary complication of acute pancreatitis.
ARDS (Acute Respiratory Distress Syndrome) is common in acute pancreatitis because severe pancreatic inflammation triggers a systemic inflammatory response, leading to lung injury characterized by increased permeability and fluid buildup in the alveoli, causing respiratory distress.
Which of the following is NOT a common cause of acute pancreatitis?
A. Biliary tract disease
B. End-stage renal disease
C. Vitamin B12 deficiency
D. High triglycerides
Correct Answer: C: ✅ Correct. While B12 is important for overall health, a deficiency does not directly cause pancreatitis.
A: ❌ Incorrect. Gallstones and biliary tract disease are among the most common causes of pancreatitis.
B: ❌ Incorrect. End-stage renal disease can contribute to pancreatitis.
D: ❌ Incorrect. High triglycerides (dyslipidemia) are a well-known cause of acute pancreatitis.
Acute pancreatitis
* Nutritional deficiencies
Micronutrient abnormalities are common
* Can be exacerbated by chronic alcohol consumption
B1, B2, B3, B9, B12, Vitamin C, Vitamin A, & zinc
* Hypocalcemia & hypomagnesemia
Saponification of calcium during fat necrosis
Are you sure B12 deficiency does not cause pancreatitis?
Yes, I’m sure. While B12 deficiency is linked to overall poor health and neuropathies, it does not directly cause pancreatitis. The nutritional deficiencies mentioned (B1, B2, B3, B9, B12, etc.) are common in pancreatitis, especially in chronic alcoholics, but they are not causative factors. Instead, gallstones, alcohol, hypertriglyceridemia, and end-stage renal disease are direct causes.
Which of the following drugs can contribute to acute pancreatitis?
A. NSAIDs, tetracycline, corticosteroids
B. Beta-blockers, acetaminophen, iron supplements
C. Aspirin, omeprazole, folic acid
D. Vitamin D, calcium supplements, probiotics
Correct Answer: A. NSAIDs, tetracycline, corticosteroids
A: ✅ Correct. These drugs have been associated with pancreatitis due to their effects on pancreatic enzymes and inflammation.
B: ❌ Incorrect. Beta-blockers and acetaminophen are not common causes, and iron supplements are more related to gallstone formation.
C: ❌ Incorrect. Aspirin and omeprazole are not major contributors to pancreatitis.
D: ❌ Incorrect. None of these substances are known to cause pancreatitis.
**NSAIDs: **Mixed effects—some reduce pancreatic inflammation due to their anti-inflammatory properties, but some (e.g., ibuprofen, naproxen) have been associated with drug-induced pancreatitis.
**Tetracycline: **Can cause drug-induced pancreatitis by direct toxicity to pancreatic acinar cells and inducing fatty infiltration in the pancreas.
**Corticosteroids ** can induce hypertriglyceridemia
High triglycerides are a known cause of pancreatitis.
Steroids increase lipolysis (fat breakdown), releasing free fatty acids into circulation, which the liver converts into triglycerides.
If triglycerides rise above 1,000 mg/dL, they can trigger pancreatitis through pancreatic lipotoxicity.
Immunosuppression and worsening inflammation
While steroids reduce inflammation systemically, they also suppress immune responses.
In pancreatitis, an impaired immune system can allow prolonged tissue damage, increasing the risk of infections (e.g., infected pancreatic necrosis).
Instead of controlling inflammation, steroids can alter the normal healing response, prolonging the inflammatory phase rather than resolving it effectively.
Bottom Line:
Steroids don’t directly “worsen” pancreatitis inflammation, but they can increase the risk of developing pancreatitis (via hypertriglyceridemia) and impair the immune response, potentially leading to complications like infections.
Why is hyperglycemia common in acute pancreatitis?
A. Insulin resistance and β-cell damage impair glucose regulation.
B. Increased insulin production lowers blood sugar.
C. Excess glucose is rapidly excreted in urine.
D. The pancreas releases stored sugar during inflammation.
Correct Answer: A. Insulin resistance and β-cell damage impair glucose regulation.
A: ✅ Correct. Inflammation leads to insulin resistance, while pancreatic β-cell damage reduces insulin secretion.
B: ❌ Incorrect. Insulin production is impaired, not increased.
C: ❌ Incorrect. While glucose can be lost in urine in severe hyperglycemia, it’s not the main reason for high blood sugar in pancreatitis.
D: ❌ Incorrect. The pancreas does not store sugar; the liver does.
Acute pancreatitis
* Pathophysiology of malnutrition
Deteriorating nutrition status is due to multiple factors
* 1) Inflammation
TNFalpha, IL-1, IL-6
Cortisol, catecholamines, glucagon all released
Metabolic pattern similar to sepsis
* Elevated resting energy expenditure
* FYI – 111% in mild pancreatitis, 126% in severe
pancreatitis, 120% in pancreatic sepsis
* Protein catabolism (negative nitrogen balance)
* Production of acute phase proteins
* Rapid decline of muscle mass and function within 5 days without nutrition support
* Hyperglycemia
* Insulin resistance, stimulation of gluconeogenesis in the
, impaired insulin secretion from -cell damage
👉 Hyperglycemia in acute pancreatitis is caused by:
✅ Insulin resistance, increased gluconeogenesis, and β-cell damage.
Insulin resistance: Inflammation releases TNF-α, IL-1, and IL-6, which impair insulin signaling, leading to reduced glucose uptake by cells.
Increased gluconeogenesis: The body responds to stress by producing glucose from non-carbohydrate sources (protein, fat) in the liver, worsening hyperglycemia.
β-cell damage: The pancreas is responsible for producing insulin via β-cells. When these cells are inflamed or destroyed, insulin secretion is impaired, leading to uncontrolled blood sugar levels.
🔹 Summary: Acute pancreatitis triggers metabolic stress, leading to high blood sugar due to insulin resistance, excessive glucose production (gluconeogenesis), and damage to insulin-producing β-cells.
What is a severe, life-threatening complication of acute pancreatitis?
A. Bacterial pneumonia
B. Acute respiratory distress syndrome (ARDS)
C. Chronic kidney disease
D. Deep vein thrombosis (DVT)
Correct Answer: B. Acute respiratory distress syndrome (ARDS)
A: ❌ Incorrect. Pneumonia can occur, but it is not a hallmark severe complication of pancreatitis.
B: ✅ Correct. ARDS is a major life-threatening complication caused by systemic inflammation and lung involvement.
C: ❌ Incorrect. Kidney issues can occur, but they are secondary to other complications.
D: ❌ Incorrect. DVT is not a primary concern in pancreatitis.
Which of the following is NOT a complication of acute pancreatitis?
A) Chronic pancreatitis
B) Pseudocysts
C) Acute respiratory distress syndrome (ARDS)
D) Peptic ulcer disease
Correct Answer: D) Peptic ulcer disease
✅ D) Peptic ulcer disease (PUD) is incorrect because while pancreatitis and PUD may share risk factors (e.g., NSAID use), PUD is not a direct complication of pancreatitis.
❌ A) Chronic pancreatitis is incorrect because repeated episodes of acute pancreatitis can lead to long-term pancreatic damage, resulting in chronic pancreatitis.
❌ B) Pseudocysts are incorrect as they form due to pancreatic fluid collection after inflammation.
❌ C) ARDS is incorrect since severe pancreatitis can trigger systemic inflammation, leading to lung injury and ARDS.
Which of the following metabolic changes is commonly seen in acute pancreatitis?
A) Hypoglycemia
B) Insulin resistance
C) Decreased gluconeogenesis
D) Increased insulin secretion
Correct Answer: B) Insulin resistance
✅ B) Insulin resistance is correct because inflammation releases stress hormones (e.g., cortisol, catecholamines, glucagon), leading to impaired glucose uptake and increased blood sugar levels.
❌ A) Hypoglycemia is incorrect because acute pancreatitis more commonly leads to hyperglycemia due to insulin resistance and increased gluconeogenesis.
❌ C) Decreased gluconeogenesis is incorrect since gluconeogenesis is actually increased, as the body tries to compensate for stress.
❌ D) Increased insulin secretion is incorrect because pancreatic inflammation and β-cell dysfunction can impair insulin secretion rather than increase it.
What is a common cause of hypertriglyceridemia in acute pancreatitis?
A) Increased lipid catabolism and decreased lipid clearance
B) Increased pancreatic enzyme secretion
C) Increased insulin sensitivity
D) Increased bile acid production
Correct Answer: A) Increased lipid catabolism and decreased lipid clearance
✅ A) Increased lipid catabolism and decreased lipid clearance is correct because insulin resistance and pancreatic dysfunction impair the body’s ability to metabolize lipids, leading to elevated serum triglycerides.
❌ B) Increased pancreatic enzyme secretion is incorrect since pancreatic function is impaired, not overactive.
❌ C) Increased insulin sensitivity is incorrect because insulin resistance is common in acute pancreatitis, leading to impaired glucose metabolism.
❌ D) Increased bile acid production is incorrect as bile acids play a role in digestion but do not directly contribute to hypertriglyceridemia.
Acute Pancreatitis caused by Malnutrition
Hypertriglyceridemia is common
* Lipid catabolism and impaired lipid clearance from decreased insulin secretion contribute to elevated serum triglycerides
* Can also be considered a cause of acute pancreatitis
General malnutrition from decreased oral intake due to anorexia, abdominal pain, nausea/vomiting, ileus, gastroparesis, gastric outlet obstruction
* Pancreatic exocrine dysfunction can persist for 6-18
months after acute attack
What percentage of patients with acute pancreatitis go on to develop chronic pancreatitis?
A) 10%
B) 15%
C) 25%
D) 50%
Statistics after acute episode of Acute Pancreatitis
25% of patients with acute pancreatitis go on to have
chronic pancreatitis
27% experience pancreatic enzyme insufficiency, more common in alcoholic pancreatitis, severe pancreatitis, and necrotizing pancreatitis.
What is a common pathophysiological feature of chronic pancreatitis?
A) Ductal obstruction by concretions
B) Acute inflammation of the pancreas
C) Reversible destruction of pancreatic tissue
D) Excessive insulin production
Answer: A) Ductal obstruction by concretions
Explanation: One of the key features of chronic pancreatitis is ductal obstruction by concretions, which are due to increased protein concentrations in the pancreatic juice that form plugs, which can calcify. This is part of the chronic disease process.
❌ Wrong Answers:
B) Acute inflammation of the pancreas: Chronic pancreatitis is characterized by irreversible inflammation, not acute inflammation.
C) Reversible destruction of pancreatic tissue: The destruction in chronic pancreatitis is irreversible.
D) Excessive insulin production: Chronic pancreatitis typically results in reduced, not increased, insulin production due to damage to the endocrine pancreas.
Chronic pancreatitis
* Pathophysiology:
Thought to be related to multiple episodes of acute pancreatitis
Ductal obstruction by concretions – due to increased protein concentrations in the pancreatic juice, forms plugs that can become calcified
Alcohol has a toxic effect on pancreatic acinar cells
* Oxidative stress on pancreatic cells (from alcohol abuse) may result in the activation of pancreatic
Which of the following is a clinical finding in chronic pancreatitis?
A) Acute, severe abdominal pain
B) Steatorrhea only
C) Silent disease until pancreatic insufficiency or diabetes develop
D) Excessive weight gain
**Answer: C) Silent disease until pancreatic insufficiency or diabetes develop
Explanation: Chronic pancreatitis may be entirely silent until pancreatic insufficiency and diabetes mellitus develop. Early signs include mild to moderate abdominal pain, but more severe consequences like malabsorption, diabetes, and weight loss occur later.**
❌ Wrong Answers:
A) Acute, severe abdominal pain: Pain in chronic pancreatitis is usually mild to moderate and recurrent, not acute or severe.
B) Steatorrhea only: Steatorrhea is a symptom that may develop later, but not the only clinical finding.
D) Excessive weight gain: Weight loss is more common due to malabsorption and pancreatic insufficiency.
Clinical findings of Chronic Pancreatitis
Repeated attacks of mild or moderately severe abdominal pain or back pain
* The disease may be entirely silent until pancreatic insufficiency and diabetes mellitus develop
50% mortality after 25 years, usually linked to development of malabsorption and diabetes
Which is a nutritional consideration for managing chronic pancreatitis?
A) Avoid all fats
B) Correct weight loss and alleviate steatorrhea
C) Only provide high-protein foods
D) Ignore vitamin deficiencies until late stages
✅ Correct Answer: B) Correct weight loss and alleviate steatorrhea
👉 Why? The goal is to manage malabsorption, correct weight loss, and alleviate steatorrhea (fat malabsorption) in chronic pancreatitis.
❌ Wrong Answers:
A) Increase pancreatic enzyme secretion: Nutrition therapy doesn’t focus on increasing enzyme secretion but managing the effects of enzyme insufficiency.
C) Only provide high-protein foods: A balanced diet is required, not just high-protein foods.
D) Eliminate all alcohol from the diet: While alcohol should be avoided, the main focus is on managing malabsorption and correcting nutritional deficiencies
Nutritional Goals for Chronic pancreatitis
Reduce pain
Alleviate steatorrhea & diarrhea
Avoid/prevent complications
Maintain/correct weight loss
Chronic pancreatitis is typically caused by which of the following?
A) Cystic fibrosis
B) Long-term alcohol abuse
C) Acute pancreatitis only
D) Obstruction due to tumors
✅ Correct Answer: B) Long-term alcohol abuse
👉 Why? Chronic pancreatitis is most often caused by long-term alcohol abuse, which leads to repeated acute pancreatitis episodes.
❌ Wrong Answers:
A) Cystic fibrosis: While cystic fibrosis can contribute to chronic pancreatitis, it is less common than alcohol abuse.
C) Acute pancreatitis only: Chronic pancreatitis is usually a result of multiple episodes of acute pancreatitis.
D) Obstruction due to tumors: While obstruction can contribute, long-term alcohol abuse is the primary cause of chronic pancreatitis.
How does alcohol cause pancreatitis?
Alcohol triggers pancreatitis through multiple mechanisms:
Toxic effects on acinar cells → Direct damage to pancreatic cells leads to enzyme activation within the pancreas, causing self-digestion.
Increased zymogen secretion → Alcohol stimulates enzyme production but reduces bicarbonate secretion, making the pancreatic fluid thicker and prone to blockage.
Oxidative stress → Leads to inflammation and fibrosis over time.
Sphincter of Oddi dysfunction → Alcohol can cause spasms of the sphincter, leading to enzyme backup and pancreatic auto-digestion.
This leads to progressive fibrosis and pancreatic enzyme insufficiency (PEI), as the pancreas loses its ability to produce digestive enzymes.
Why is Alcoholic Pancreatitis associated with Pancreatic Enzyme Insufficiency?
A) Mild pancreatitis
B) Alcoholic pancreatitis
C) Acute pancreatitis only
D) Cystic fibrosis
✅ Correct Answer: B) Alcoholic pancreatitis
👉 Why? Chronic alcohol consumption causes repeated inflammation of the pancreas, leading to progressive damage. This results in fibrosis (scarring) and loss of pancreatic acinar cells, which are responsible for producing digestive enzymes. Over time, this leads to pancreatic enzyme insufficiency (PEI), meaning the pancreas cannot produce enough enzymes to aid digestion properly.
❌ Wrong Answers:
A) Mild pancreatitis: Mild cases do not typically cause long-term pancreatic damage, so enzyme insufficiency is rare.
C) Acute pancreatitis only: Acute episodes may cause temporary inflammation, but they do not always lead to lasting enzyme insufficiency. Chronic damage is needed for insufficiency to develop.
D) Cystic fibrosis: While cystic fibrosis can lead to pancreatic insufficiency, the text emphasizes that alcohol-related pancreatitis is a more common cause in adults.
2) What is the difference between Endocrine and Exocrine?
The pancreas has both endocrine and exocrine functions, meaning it plays two different roles in the body.
Hint: think endo - stays in the body which is why it is the things that secrete into the blood stream
Exo- exits the body which is why it is secreted in the GI tract
Key Differences:
Endocrine = Releases hormones directly into the bloodstream (e.g., insulin for blood sugar control).
Exocrine = Releases digestive enzymes into the small intestine (duodenum) to break down food.
In chronic pancreatitis, both functions can become impaired, leading to:
Exocrine insufficiency → Malabsorption, weight loss, and steatorrhea (fatty stools) due to enzyme deficiency.
Endocrine insufficiency → Diabetes mellitus due to damage to insulin-producing cells.
Endocrine = Secretes into the blood (hormones that regulate body functions)
Example: Insulin (lowers blood sugar) & Glucagon (raises blood sugar) from the pancreas
Exocrine = Secretes into the GI tract (or other body surfaces like skin)
Example: Digestive enzymes (lipase, amylase, proteases) from the pancreas into the small intestine
So, if something is released into the bloodstream, it’s endocrine. If it’s released into a duct or an organ like the GI tract, it’s exocrine.
Case 1: Initial Presentation
A 42-year-old female presents with on-and-off upper right abdominal pain for 4 months, worsened after eating. She also reports loose bowel movements, gas, and bloating, but no jaundice or fever. Palpation of the liver area causes mild discomfort.
1) What is the most appropriate next step in diagnosing this patient?
A) Perform an ultrasound
B) Prescribe pancreatic enzyme replacement therapy (PERT) immediately
C) Order a CT scan of the abdomen
D) Refer for immediate gallbladder removal
✅ Correct Answer: A) Perform an ultrasound
👉 Why? Given her upper right abdominal pain and digestive symptoms, an ultrasound is the best initial imaging to assess for gallbladder disease (e.g., gallstones, sludge).
❌ Wrong Answers:
B) Prescribe PERT immediately: Without confirming pancreatic insufficiency, enzyme therapy is premature.
C) Order a CT scan: A CT is not first-line for suspected gallbladder issues—ultrasound is preferred.
D) Refer for gallbladder removal: Surgery isn’t needed unless symptoms worsen significantly or complications arise.
Chronic Kidney Disease (CKD) Diagnosis & Management
1) How is chronic kidney disease (CKD) diagnosed?
A) Based on serum creatinine levels only
B) Based on estimated glomerular filtration rate (eGFR)
C) Only when a patient requires dialysis
D) Only when kidney stones are present
✅ Correct Answer: B) Based on estimated glomerular filtration rate (eGFR)
👉 Why? CKD is classified into 5 stages based on eGFR, which measures how well the kidneys filter waste from the blood.
❌ Wrong Answers:
A) Based on serum creatinine levels only: Creatinine is used to estimate eGFR, but eGFR is the main diagnostic tool.
C) Only when a patient requires dialysis: CKD is diagnosed long before dialysis is needed (early stages 1-4).
D) Only when kidney stones are present: Kidney stones are not necessary for CKD diagnosis and are a separate condition.
Chronic kidney disease
- Chronic kidney disease (CKD) is diagnosed based on eGFR levels
- Divided into 5 categories
- Category 5 (also known as End-Stage renal disease (ESRD)) is when dialysis is generally recommended. GFR <15
- Diet is critical to management of ESRD during regular dialysis
2) When is dialysis generally recommended for CKD patients?
A) When eGFR is below 15 mL/min
B) As soon as eGFR drops below 60 mL/min
C) Only when a patient develops high blood pressure
D) If a patient has protein in their urine
✅ Correct Answer: A) When eGFR is below 15 mL/min
👉 Why? End-stage renal disease (Stage 5 CKD) occurs when GFR <15 mL/min, meaning the kidneys cannot filter waste effectively, and dialysis is needed.
❌ Wrong Answers:
B) As soon as eGFR drops below 60 mL/min: Stages 1-3 CKD do not require dialysis—only monitoring and lifestyle changes.
C) Only when a patient develops high blood pressure: High BP is a risk factor for CKD but does not determine when dialysis is needed.
D) If a patient has protein in their urine: Proteinuria is a sign of kidney damage, but it does not mean dialysis is required yet.
3) What is the main goal of dialysis?
A) To cure kidney disease
B) To remove uremic toxins and balance fluid levels
C) To replace the need for kidney transplants
D) To remove blood from the body permanently
✅ Correct Answer: B) To remove uremic toxins and balance fluid levels
👉 Why? Dialysis filters waste, removes excess fluid, and balances electrolytes to compensate for kidney failure.
❌ Wrong Answers:
A) To cure kidney disease: Dialysis does not cure CKD—it manages symptoms while awaiting transplant or continued treatment.
C) To replace the need for kidney transplants: Dialysis is a temporary or long-term treatment, but transplants offer a permanent solution for some patients.
D) To remove blood from the body permanently: Dialysis cleans the blood and returns it to the body—it does not remove it permanently.
4) Which nutrients should be restricted in dialysis patients?
A) Potassium, phosphorus, sodium, fluid
B) Protein, vitamin C, calcium
C) Iron, vitamin B12, omega-3 fatty acids
D) Carbohydrates, fiber, zinc
✅ Correct Answer: A) Potassium, phosphorus, sodium, fluid
👉 Why? Dialysis patients need to limit these to prevent fluid overload, bone disease, and heart complications.
❌ Wrong Answers:
B) Protein, vitamin C, calcium: Protein is needed for muscle maintenance, vitamin C is not restricted, and calcium should be managed but not fully restricted.
C) Iron, vitamin B12, omega-3 fatty acids: Iron and B12 are often supplemented to manage anemia in CKD patients.
D) Carbohydrates, fiber, zinc: Carbohydrates and fiber are not restricted, and zinc is sometimes supplemented in CKD patients.
Chronic kidney disease
- Main goals of diet:
- Minimize accumulation of toxic compounds not adequately removed via dialysis
- Prevent malnutrition
- Diet includes restrictions of potassium, phosphorus, sodium and fluid
- Risk for deficiency of several nutrients
Dialysis Types: Peritoneal vs. Hemodialysis
5) Which statement about peritoneal dialysis (PD) is true?
A) PD uses a machine to filter blood in a clinic
B) PD is more commonly used than hemodialysis
C) PD uses the peritoneal cavity as a filter
D) PD is recommended for patients with abdominal hernias
✅ Correct Answer: C) PD uses the peritoneal cavity as a filter
👉 Why? PD uses the body’s own peritoneal membrane to filter waste using a hyperosmolar solution.
❌ Wrong Answers:
A) PD uses a machine to filter blood in a clinic: This describes hemodialysis (HD), not PD.
B) PD is more commonly used than hemodialysis: HD is more common; PD is less frequently used.
D) PD is recommended for patients with abdominal hernias: PD is not ideal for abdominal issues like hernias or adhesions.
Peritoneal Dialysis (PD)
Uses body’s peritoneal cavity as an “artificial dialyzer” and filters the blood using a hyperosmolar solution
2 Types
1. Continuous ambulatory PD – does not require a machine and filters blood 24/7
2. Automated PD (Continuous cycling PD) – requires machine to fill and drain abdomen usually during sleep
PD is not commonly used
6) Which patient would be a better candidate for hemodialysis (HD) over PD?
A) A patient with severe renal impairment
B) A patient with weak blood vessels
C) A patient with an active lifestyle
D) A patient who prefers at-home treatment
✅ Correct Answer: A) A patient with severe renal impairment
👉 Why? HD is preferred for severe kidney failure because it provides more efficient filtration than PD.
❌ Wrong Answers:
B) A patient with weak blood vessels: PD is better for those who cannot tolerate vascular access.
C) A patient with an active lifestyle: PD is easier to maintain with an active lifestyle.
D) A patient who prefers at-home treatment: PD is more commonly used at home, though HD can also be done at home.
Hemodialysis (HD)
Used more frequently than PD and treats advanced and permanent kidney failure
Blood flows through a filter and removes wastes and extra fluids before being returned to the body
Less protein is lost with HD then PD but can still loose amino acids
Hemodialysis (HD) VS. Peritoneal dialysis (PD)
Doctor may recommend PD if patient doesn’t have strong blood vessels to withstand hemodialysis. It is generally easier to maintain everyday activities
HD would be preferred for patients with any abdominal concerns such as inflammatory bowel diseases, hernias, adhesions or obesity
HD is the preferred option for severe renal impairment Research shows life expectancy is similar with both types
Dialysis Side Effects
7) What is a common side effect of dialysis?
A) Low blood pressure
B) Increased kidney function
C) Higher energy levels
D) Increased urine output
✅ Correct Answer: A) Low blood pressure
👉 Why? Removing too much fluid too quickly can cause low blood pressure, leading to dizziness, nausea, or fainting.
❌ Wrong Answers:
B) Increased kidney function: Dialysis does not restore kidney function—it compensates for lost function.
C) Higher energy levels: Many dialysis patients experience fatigue and malnutrition.
D) Increased urine output: Most CKD patients in later stages produce very little urine.
Dialysis common side effects
- Low blood pressure – can cause dizziness, nausea or fainting
- Muscle cramping – when fluid is removed too quickly
- Itchy Skin
- Sleep concerns- restless leg
- Anemia
- Bone concerns – damaged kidneys can’t metabolize vitamin D
- High phosphate – can contribute to bone concerns and skin itching
- Hypokalemia – low potassium can cause fatigue, weakness, heart palpitations, constipation
- Primary (Idiopathic) RLS
Genetic predisposition: Often runs in families, with symptoms typically appearing before age 40.
Dysfunction in dopamine pathways: Dopamine regulates movement, and abnormalities can lead to the sensations associated with RLS. - Secondary Causes of RLS
Iron Deficiency:
Low serum ferritin (<50 ng/mL) is strongly linked to RLS.
Iron is essential for dopamine synthesis in the brain.
Chronic Kidney Disease (CKD) & End-Stage Renal Disease (ESRD):
Common in dialysis patients due to iron deficiency, uremia, and metabolic disturbances.
Pregnancy (especially third trimester):
Possibly due to iron deficiency, hormonal changes, and increased blood volume.
Neurological Disorders:
Parkinson’s disease (dopamine dysregulation).
Multiple sclerosis (MS).
Peripheral neuropathy:
Diabetes, alcoholism, or nerve damage can trigger RLS symptoms.
Medications that Worsen RLS:
Antihistamines (e.g., diphenhydramine, hydroxyzine).
Antipsychotics (e.g., haloperidol, risperidone).
SSRIs & SNRIs (e.g., fluoxetine, venlafaxine).
Dopamine antagonists (e.g., metoclopramide).
Caffeine, Nicotine, and Alcohol:
Can disrupt dopamine function and worsen symptoms.
Bottom Line
If no clear secondary cause is found, primary RLS is likely due to dopamine dysfunction and genetic predisposition.
Checking iron levels (serum ferritin) is crucial since supplementation can help in many cases.
Identifying and avoiding triggers (certain medications, caffeine, alcohol) is also key.
Iron plays a crucial role in dopamine metabolism, and its deficiency can contribute to the development of Restless Leg Syndrome (RLS) through several mechanisms:
- Iron is Essential for Dopamine Production
The brain’s dopaminergic system is involved in movement control, and dysfunction in this system is linked to RLS.
Iron is a cofactor for tyrosine hydroxylase, the enzyme that converts tyrosine to L-DOPA, a precursor to dopamine.
Low iron levels → Reduced dopamine synthesis → Dysregulated movement signals → RLS symptoms. - Brain Iron Deficiency (Even if Blood Iron is Normal)
CSF studies show that patients with RLS often have low iron levels in the brain, even if their blood iron levels appear normal.
This is due to impaired iron transport across the blood-brain barrier (BBB). - Iron Affects Dopamine Receptors
Low iron levels may cause dopamine receptor hypersensitivity, leading to abnormal signaling and excessive limb movements. - Increased Glutamate Activity
Studies suggest that brain iron deficiency leads to excessive glutamate activity, contributing to hyperexcitability and the sensation of restlessness.
Bottom Line
Iron deficiency disrupts dopamine function, increases brain excitability, and may impair blood-brain barrier transport, all of which contribute to RLS symptoms.
This is why iron supplementation (if ferritin <50 ng/mL) is a first-line treatment for RLS.
Electrolyte Imbalances & Dialysis
8) Why is high phosphate a concern in dialysis patients?
A) It contributes to bone disease and skin itching
B) It improves muscle function
C) It enhances kidney function
D) It reduces anemia risk
✅ Correct Answer: A) It contributes to bone disease and skin itching
👉 Why? High phosphate levels can lead to calcium imbalances, weakening bones, and itchy skin due to deposits in tissues.
❌ Wrong Answers:
B) Improves muscle function: Too much phosphate can lead to muscle weakness.
C) Enhances kidney function: Phosphate retention worsens kidney function.
D) Reduces anemia risk: Phosphate does not affect anemia—iron and erythropoietin do.
Metabolic & Cardiovascular Risks in Dialysis Patients
9) What is the leading cause of death in dialysis patients?
A) Cardiovascular disease
B) Infections
C) Malnutrition
D) Kidney cancer
✅ Correct Answer: A) Cardiovascular disease
👉 Why? Around 50% of dialysis patient mortality is due to cardiovascular disease, worsened by metabolic syndrome and electrolyte imbalances.
❌ Wrong Answers:
B) Infections: While dialysis patients are at risk of infections, cardiovascular issues are the primary cause of death.
C) Malnutrition: Malnutrition is common but not the leading cause of death.
D) Kidney cancer: CKD patients are at increased risk of cancer, but it is not the leading cause of death in dialysis patients.
Dialysis
Dialysis is a method to artificially filter the blood Approximately 30% of dialysis patients are diabetic
50% mortality of these patients is attributed to cardiovascular disease
Metabolic syndrome increases the risk
Dialysis & Muscle Wasting
Why are dialysis patients at risk for malnutrition?
A) Dialysis is a catabolic process
B) Dialysis improves kidney function and removes excess protein
C) Dialysis patients eat too much protein
D) The body absorbs too many nutrients during dialysis
✅ Correct Answer: A) Dialysis is a catabolic process
👉 Why? Dialysis breaks down proteins and removes amino acids, leading to muscle loss (cachexia) and nutritional decline.
❌ Wrong Answers:
B) Dialysis improves kidney function and removes excess protein: Dialysis does not improve kidney function; it filters waste but also removes essential nutrients.
C) Dialysis patients eat too much protein: Protein intake is carefully managed, but many patients struggle with low protein intake due to appetite suppression.
D) The body absorbs too many nutrients during dialysis: The opposite is true—nutrient loss occurs during dialysis.
Dialysis
Kidney failure leads to toxin accumulation – this causes appetite suppression and contributes to nutritional decline
Dialysis is a catabolic process so patients can suffer from varying degrees of malnutrition
Can see cachexia, metabolic and mineral concerns
Home Hemodialysis (HD) vs. In-Center HD
12) What is a key advantage of home hemodialysis (HD)?
A) More frequent, shorter sessions can be more effective
B) Does not require training for the patient or family
C) Eliminates the need for vascular access
D) Reduces the need for dietary restrictions
✅ Correct Answer: A) More frequent, shorter sessions can be more effective
👉 Why? Home HD is typically 6-7 days per week for ~2 hours per session, allowing better toxin removal and more stable fluid balance.
❌ Wrong Answers:
B) Does not require training for the patient or family: Home HD requires extensive training for safety and emergency handling.
C) Eliminates the need for vascular access: A port or fistula is still required for home HD.
D) Reduces the need for dietary restrictions: Patients still need dietary restrictions, especially for sodium, potassium, and phosphorus.
Hypokalemia & Other Electrolyte Issues in Dialysis
13) Why is hypokalemia (low potassium) a concern in dialysis patients?
A) It can cause fatigue, weakness, and heart palpitations
B) It improves dialysis efficiency
C) It increases calcium absorption
D) It prevents fluid retention
✅ Correct Answer: A) It can cause fatigue, weakness, and heart palpitations
👉 Why? Potassium is essential for muscle and nerve function, and low levels can cause heart rhythm disturbances.
❌ Wrong Answers:
B) It improves dialysis efficiency: Hypokalemia does not improve dialysis—it can be dangerous.
C) It increases calcium absorption: Potassium does not regulate calcium absorption.
D) It prevents fluid retention: Sodium and albumin play a greater role in fluid balance, not potassium.
1) Why is constipation a concern in dialysis patients?
A) Dialysis causes excessive bowel movements
B) Fluid restrictions in dialysis patients can lead to constipation
C) Patients consume too much fiber
D) Sodium intake prevents constipation
✅ Correct Answer: B) Fluid restrictions in dialysis patients can lead to constipation
👉 Why? Dialysis patients have restricted fluid intake, which can lead to dehydration and constipation.
❌ Wrong Answers:
A) Dialysis causes excessive bowel movements: Dialysis does not cause diarrhea, and constipation is more common.
C) Patients consume too much fiber: Dialysis patients often do not get enough fiber.
D) Sodium intake prevents constipation: Excess sodium can contribute to dehydration, which worsens constipation.
Magnesium in Chronic Kidney Disease (CKD) & Dialysis
Why do patients with End-Stage Renal Disease (ESRD) not on dialysis often have hypermagnesemia?
A) The kidneys cannot effectively excrete magnesium
B) Dialysis patients absorb too much magnesium
C) Magnesium is lost during dialysis, leading to hypermagnesemia
D) Magnesium is rarely found in foods, making excess intake unlikely
✅ Correct Answer: A) The kidneys cannot effectively excrete magnesium
👉 Why? Damaged kidneys cannot remove magnesium, leading to high serum magnesium levels in non-dialysis ESRD patients.
❌ Wrong Answers:
B) Dialysis patients absorb too much magnesium: Dialysis can lower magnesium levels, depending on the dialysate.
C) Magnesium is lost during dialysis, leading to hypermagnesemia: Magnesium is not lost in excess, and dialysis can help regulate levels.
D) Magnesium is rarely found in foods: Magnesium is found in many foods, and poor kidney function is the main issue.
Chronic kidney disease - magnesium
- Patients with end stage renal disease not on dialysis frequently present with hypermagnesemia – kidney can’t excrete effectively
- During dialysis serum levels of magnesium vary depending on the dialysate concentration – 0.5mmol/L usually has a normal serum level
- 0.5mmol/L plus oral supplementation 250mg magnesium 3 times/week decreased progression of arterial calcification
- Magnesium should be used cautiously in dialysis patients and serum levels should be monitored regularly
3) What is the recommended daily sodium intake for hemodialysis patients?
A) 1000 mg
B) 1500-2000 mg
C) 2300 mg
D) 4000 mg
✅ Correct Answer: B) 1500-2000 mg
👉 Why? Some guidelines recommend 1500-2000 mg/day, though other references suggest 2300 mg as an upper limit.
❌ Wrong Answers:
A) 1000 mg: This may be too low to meet basic physiological needs.
C) 2300 mg: This is acceptable but higher than optimal for most dialysis patients.
D) 4000 mg: Too high—this would increase fluid retention and blood pressure.
Hemodialysis- sodium
- Chart above lists sodium at 2300mg. Other references site 1500-2000mg/day is optimal during dialysis
- To maintain this level council patients to
- Stop adding salt to cooking
- Don’t add extra salt to foods- don’t keep salt on the table
- Avoid processed foods with high sodium levels
4) What is the recommended fluid intake for hemodialysis patients?
A) 1-2 liters per day
B) 750-1000 mL plus urine output
C) 3-4 liters per day
D) No restrictions are needed
✅ Correct Answer: B) 750-1000 mL plus urine output
👉 Why? This helps control fluid retention and prevents excessive weight gain between dialysis treatments.
❌ Wrong Answers:
A) 1-2 liters per day: Too high for many dialysis patients.
C) 3-4 liters per day: Excessive and dangerous—can lead to fluid overload.
D) No restrictions are needed: Strict fluid control is crucial in dialysis patients.
Vitamin K & Hemodialysis
Why are hemodialysis patients at risk for vascular calcification?
A) Vitamin K deficiency affects matrix Gla protein, which inhibits calcification
B) Vitamin K supplements are harmful in dialysis patients
C) Dialysis removes too much vitamin K
D) Vascular calcification is unrelated to dialysis
✅ Correct Answer: A) Vitamin K deficiency affects matrix Gla protein, which inhibits calcification
👉 Why? Matrix Gla protein is vitamin K-dependent, and its deficiency accelerates arterial calcification.
❌ Wrong Answers:
B) Vitamin K supplements are harmful in dialysis patients: There is no evidence that vitamin K supplements are harmful.
C) Dialysis removes too much vitamin K: Dialysis does not significantly remove vitamin K.
D) Vascular calcification is unrelated to dialysis: Dialysis patients have an increased risk of vascular calcification.
How might essential fatty acid (EFA) supplementation help dialysis patients?
A) It prevents vascular calcification
B) It improves dialysis efficiency
C) It reduces pruritus (itching)
D) It increases sodium absorption
✅ Correct Answer: C) It reduces pruritus (itching)
👉 Why? 80% of dialysis patients experience pruritus, and EFAs help improve skin hydration and reduce itching.
❌ Wrong Answers:
A) It prevents vascular calcification: EFAs are not directly involved in vascular calcification.
B) It improves dialysis efficiency: EFAs do not impact dialysis filtration efficiency.
D) It increases sodium absorption: EFAs do not affect sodium absorption.
Hemodialysis- EFA’s
- 80% of dialysis patients experience pruritus which can become severe
- Essential fatty acid (EFA) deficiency may contribute
- DBT with evening primrose oil (EPO) -10ml bid (640mg of gamma-linolenic acid) showed improvements
- Another trial – 1 g bid of EPO showed improvement in pruritus, dryness and erythema
- 3g/day fish oil (18% EPA and 12% DHA)- for 20 days improved pruritus
How is iron loss in CKD patients. And why is iron levels a concern for CKD patients.
- Increased Blood Loss
Frequent blood draws: CKD patients undergo regular blood tests, leading to gradual iron depletion.
GI bleeding: Uremia (high toxin levels due to kidney dysfunction) can cause gastritis and GI ulcers, leading to chronic blood loss.
Dialysis-related blood loss:
Blood gets trapped in the dialysis tubing.
Heparin (used to prevent clotting in dialysis) can increase bleeding risk. - Reduced Iron Absorption
Inflammation from CKD increases hepcidin, a liver hormone that blocks iron absorption in the gut and traps iron in storage, making it unavailable for red blood cell production. - Erythropoietin (EPO) Deficiency
The kidneys produce EPO, a hormone that stimulates red blood cell production.
In CKD, low EPO → reduced RBC production → anemia.
The body tries to compensate by using more iron to make RBCs, leading to depletion. - Increased Iron Demand from ESA Therapy
CKD patients often receive erythropoiesis-stimulating agents (ESAs) (e.g., epoetin alfa) to boost RBC production.
This increases iron demand, leading to iron depletion if intake or stores are insufficient.
Bottom Line
CKD causes iron loss due to blood loss, impaired absorption, inflammation, reduced EPO production, and increased iron demand from ESA therapy. This contributes to anemia of CKD, which is commonly treated with iron supplementation and EPO therapy.
