pathophys- essay 5

Abnormal Digestion and Absorption of Lipids

Abnormal Digestion and Absorption of Lipids

Occurs due to:

• Decreased bile salts

• Decreased pancreatic lipase production - low BP (BILE, PANCREATIC)

• High dietary calcium and magnesium → form insoluble soaps with fatty acids and bile salts, impairing absorption. - MC IS BF (MICHEAL IS BF)

• Diarrheal syndromes → shortened intestinal transit time - comes out faster

• Hypovitaminosis → reduced fat utilization due to deficiency of fat-soluble vitamins

• Protein starvation → impaired lipoprotein synthesis and transport, causing defective lipid absorption and fatty liver (just low protein synth and transp, meaning low prot abs (STA) but add lipo

LOW BP, MC = IS + BF, PHD (PS fatty, HAS DIARr)

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Lipoproteins

Lipoproteins - CHIL V! (chill vi) but the actual order is C VIL H

Transport lipids in the blood.

Chylomicrons

• Transport dietary triglycerides and cholesterol from intestine to tissues (chylo, kyle works in IT) int to tiss.

VLDL (Very Low-Density Lipoproteins) TLT

• Transport triglycerides from liver to tissues ( NOT CHOLESTEROL< TRIGLIDERISED_

IDL (Intermediate-Density Lipoproteins)

• VLDL remnants

• Precursors of LDL

LDL (Low-Density Lipoproteins)

• Transport cholesterol to tissues

• "Bad cholesterol"

HDL (High-Density Lipoproteins)

• Reverse cholesterol transport to liver -sends it back to liver

• "Good cholestero

Disordered Lipid TransportDisordered Lipid Transport

Disordered Lipid Transport

Occurs when lipoprotein production, utilization, or clearance is disturbed.

Leads to dyslipidemias and atherosclerosis.

L - PUCD (LIKE L PUKED), LEADS TO NEXT TWO PARTS OF THE ESSAS

Genetic Causes - GAF

Familial Hypercholesterolemia dR Pallavi

• Defective/absent LDL receptors

• Reduced LDL clearance

• Plasma LDL increased

Apolipoprotein E Defects - ICIC

• Impaired clearance of IDL and chylomicron remnants

Secondary Causes - HD ( SUCK HIRAS DICK, THEN H EXAMPLE WILL COME TO YOU)

Diabetes mellitus → insulin resistance increases hepatic VLDL production and reduces HDL. (IR INCREASES VI, DECREASES HIRA) IR = bc hiras mum has it like shes used to it putting hira down but it pushes ME UP to motivate me for gym (IRVH)

Hypothyroidism → reduced LDL receptor activity raises LDL cholesterol. (same as family)

other causes: Obesity, alcohol excess, and diets high in saturated fats also contribute to abnormal lipid transport.

Dyslipidemias

Dyslipidemias

Abnormal concentrations of lipoproteins in blood.

HC - HI CHETHAN

HT - HARSH THANKI COMES SECOND

MD - GETS HIS MD THO

LH (L harsh - for coming second)

L - LAYA

VT - VANI THRISHA

LT - LAYA THRISHA

Hypercholesterolemia

• ↑ LDL cholesterol

Hypertriglyceridemia

• ↑ VLDL and triglycerides

Mixed Dyslipidemia

• ↑ LDL + ↑ triglycerides

• Common in metabolic syndrome and type 2 diabetes

Low HDL Cholesterol - CAR (cad, arth, REVERSE HTINGY REDUCED)

• Independent risk factor for CAD and atherosclerosis

• Reduces reverse cholesterol transport and antioxidant activity

To increase HDL:

• Smoking cessation

• Weight loss

• Physical activity

• Niacin

Atherosclerosis

Atherosclerosis - CPD

narrowing of artieries due to infalammation, fibrous plaque formation, intimal blah blah: its like saying FIILD

• Intimal lipid deposition

• Inflammation

• Fibrous plaque formation

Pathogenesis - ENGLISH LIVES MATTER FOR SURE PALLU!!

1. Endothelial injury (hypertension, smoking, hyperlipidemia, diabetes, toxins)

2. LDL infiltration and oxidation in subendothelial space ( L I O S E) ldl, ox, sub endo)

3. Monocyte adhesion and migration → MAM/ macrophages → uptake of oxidized LDL → foam cells MUOLF

4. Fatty streak formation (earliest visible lesion)

5. Smooth muscle migration and proliferation → collagen deposition → fibrous cap formation ( SO MANY MPS, CAN DIE, FROM CUM)

6. Plaque calcification, rupture, or thrombosis → myocardial infarction, stroke. PCTR ( PALLU CHETHAN THRISH RIDE, → MS

Risk FactorsModifiable - sholds

• High LDL

• Low HDL

• Hypertension

• Diabetes mellitus

• Smoking

• Obesity

• Sedentary lifestyle

Non-Modifiable - fam

• Age

• Male sex (more common in males)

• Family history

explanation of 3:

our complete memory chain looks excellent now:

1. Monocyte adhesion and migration (Monocytes enter the wall)

2. Macrophages (Monocytes change into hunter cells)

3. Uptake of oxidized LDL (They eat the bad cholesterol)

4. Foam cell formation (They turn into fat-filled foam cells)

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