121 - Finals Cram Points

Formed elements of blood

1.     RED BLOOD CELLS	transport O2 from Lungs to Tissue and CO2 from tissue to lungs Biconcave, no nucleus, w/ hemoglobin
2.     WHITE BLOOD CELLS	defense of immune system vs. pathogens w/ nucleus, no hemoglobin, larger than rbc
3.     PLATELETS	Blood clotting Small, no nucleus

Hematopoietic Growth Factors

1.     ERYTHROPOITIN (EPO)	Produce rbc Tx for anemia in px w/ ckd, cancer and other diases causing low rbc
2.     THROMBOPOIETIN (TPO)	Produce megakaryocytes → platelets Tx for px w/ low platelet count
3.     CYTOKINES	Produce general blood cells in bone marrow Improve immune response

Characteristics of Blood Cells

1.     ERYTHROCYTES (RBC)	Anucleated (no nucleus); niconcave, w/ hemoglobin (red) Normal values: 5.4 mil per uL (male) and 4.8 mil per uL (female)
2.     LEUKOCYTES (WBC)	Only complete cell No HgB Normal values: 5,000-10,000/mm3   1.     Granulocytes – w/ granules on cytoplasm which plays important role on immune response; basophils. Eosinophils, neutrophils 2.     Agranulocytes – no granules, smooth appearance; lymphocytes
3.     THROMBOCYTES (PLATELETS)	Fragment of megakaryocytes Disc shape, granulated, anucleated Normal value: 150,000-400,000

Hematopoiesis

HEMATOPOIESIS – formation and maturation of blood in bone marrow

-        Pluripotent stem cells  myeloid and lymphoid stem cells

o   Pluripotent – immature cells

-        Myeloid  precursor cells  progenitor cells

o   Precursor cells – develop into formed elements of blood

o   Progenitor cells – no longer divide, differentiate into formed elements

-        Lymphoid  lymphocytes

Methemoglobin

iron in hemoglobin becomes Ferric (instead of Ferrous) and will not bind effectively to oxygen → cyanosis, hypoxia, death

Blood laboratory tests: Reticulocyte count

DESCRIPTION	RESULTS
% reticulocyte (immature rbc), rate of erythropoiesis Normal: 0.5-1.5%	Reticulopodia Reticulocytosis

Blood laboratory tests: Hematocrit

DESCRIPTION	RESULTS
% rbc Normal: 38-46% (male) and 35-44% (fem)	Anemia Polycythemia (>65%)

Blood laboratory tests: Mean Corpuscular Volume (MCV)

DESCRIPTION	RESULTS
Average RBC size Normocytic: 80-100 femtoliters)	Microcytic Macrocytic

Blood laboratory tests: Mean Cell Hemoglobin (MCH)

DESCRIPTION	RESULTS
Average hemoglobin per RBC Normal: 27-31 picograms/cell

Blood laboratory tests: Mean Corpuscular Hemoglobin Concentration

DESCRIPTION	RESULTS
Ave. hgb per volume of rbc Normochromic: 32-36 g/dL	Hypochromic (light) Hyperchromic (dark, no white middle)

Blood laboratory tests: RBC Distribution Width

DESCRIPTION	RESULTS
Variation of size in RBC Normal: 10.5-15%	Anisocytosis – increased, wide variation Poikilocytosis – abnormal variation Acanthocytes – thorn Cococytes – dark center Dacrocytes – pear or tear Drepanocytes – sickle Echinocytes – short thorn Elliptocytes – elliptical

Blood laboratory tests: Erythrocyte Sedimentation Rate

DESCRIPTION	RESULTS
Rate at which RBC settle For unexplained conditions (test for inflame, autoimmune or cancer) Normal: 20 (M) and 30mm/hr (F)

Blood laboratory tests: Pregnancy test

DESCRIPTION	RESULTS
Detect human chorionic gonadotrophin (hCG) Detect pregnancy 6-8 days after ovulation

Normal Hemoglobin Types

1.     HbA – in healthy adults

2.     HbF – in newborn, decrease throughout life

Abnormal Hemoglobin Types

1.     HbS – mutation in beta globin chains

a.     HbAS – only one chain

b.     HbSS – both chain

Hemostasis

1.     Vascular Spasm	Vascular smooth muscle contracts when arteries or arterioles are damaged to reduce loss of blood
2.     Platelet Plug Formation	a.     Platelet adhesion – platelet sticks together b.     Platelet release reaction – provide energy for platelet plug formation i.                TXA2 (thromboxane 2) ii.               5HT (Serotonin) -- happiness iii.              ADP (Adenosine Diphosphate) – motivation c.     Platelet Aggregation – platelet accumulate and attach
3.     Coagulation	Blood clot

Coagulation Pathways: Intrinsic

INTRINSIC PATHWAY

In blood Activated by trauma in blood Factor 12, 11, 9, 8  10 Slower

Coagulation Pathways: Extrinsic

EXTRINSIC PATHWAY

Outside of blood Activated by vascular tissue trauma Factor 3, 7  10 Quicker

Coagulation Pathways: Common

COMMON PATHWAY

Both in and out Result in stable fibrin clot Factor 10, 8, 5, 2, 1

Clotting Factor 1

I	Fibrinogen

Clotting Factor 2

II	prothrombin

Clotting Factor 3

III	Thromboplastin

Clotting Factor 4

IV

Calcium

Clotting Factor 5

V	Accelerate / labile factor

Clotting Factor 7

VII	Conversion / Stable

Clotting Factor 8

VIII	Von Willebrand / Antihemophilic A

Clotting Factor 9

IX	Christmas / Plasma thromboplastin / Antihemophilic B

Clotting Factor 10

X	Stuart / Prower / Throombokinase

Clotting Factor 11

XI	Antecedent / Antihemophilic C

Clotting Factor 12

XII	Hageman / Glass / Contact / Antihemophilic D

Clotting Factor 13

XIII	Fibrin-stabilizing

Hemostatic control mechanism: Fibrinolysis

Hemostatic control mechanism: Fibrinolysis

Fibrinolysis

Breakdown clots Plasmin dissolve CF 1, 2, 5, 8, 12

Hemostatic control mechanism: Plostacyclin

Prostacyclin (Prostaglandin I2)

Endothelial cells and WBC oppose TXA2  vasodilation, inhibit platelet adhesion

Hemostatic control mechanism: Anticoagulants

Anticoagulants

Inhibits clots -        Antithrombin 3  blocks CF 2, 9, 10, 11, 12 -        Heparin   combine with AT3 -        Protein C  inactivate CF 5, 8

Hemostatic control mechanism: Alpha 2 macroglobulin

Alpha 2 macroglobulin

Inactivate thrombin and plasmin

Hemostatic control mechanism: Alpha 1 antitrypsin

Alpha 1 antitrypsin

Inhibit CF 11

Hemostatic disorder: Thrombocytopenia

1.     Thrombocytopenia

Decrease in platelet count

Hemostatic disorder: Hemophilia

1.     Hemophilia

Absence of clotting factor (cause bruises, muscle and joint bleeding)   Hemophilia A  CF 8 Hemophilia B  CF 9 Hemophilia C  CF 11

Hemostatic disorder: Intravascular clots

1.     Intravascular clots

Roughened surface of BV due to induced platelet adhesion   Thrombus – clot in bv Emboli – dislodged thrombus to other parts of body, cause air bubbles

Hemostatic disorder: Von Willebrand’s Disease

1.     Von Willebrand’s Disease

CF 8 deficiency

Hemostatic disorder: Multiple myeloma

1.     Multiple myeloma

Cancerous disorder of plasma cells

Hemostatic disorder: Thrombocytosis

1.     Thrombocytosis

Increase in platelet count

Anemia

ANEMIA

Fatigue, intolerance to cold (low O2 for ATP), paleness (low hgb), syncopy General test: MCV and MCH

Types of anemia: Iron Deficiency Anemia

DESCRIPTION	CAUSE	S/X	DIAGNOSIS AND TX
Most prevalent Microcytic, hypochromic	Low on iron -        Diet (vegans) -        Metabolic demand (pregnancy) -        Menstruation and blood donation

Types of anemia: PERNICIOUS ANEMIA

DESCRIPTION	CAUSE	S/X	DIAGNOSIS AND TX
Macrocytic, megaloblastic	Inability to produce intrinsic factor (decrease absorption of Vit 12 needed for erythropoiesis) -        Liver disease, alcoholism, hypothyroidism

Types of anemia: HEMORRHAGIC ANEMIA

DESCRIPTION	CAUSE	S/X	DIAGNOSIS AND TX
Acute – from heavy bleeding (mens, large wounds) Chronic – prolonged bleeding (stomach ulcer)	Bleeding

Types of anemia: HEMOLYTIC ANEMIA

DESCRIPTION	CAUSE	S/X	DIAGNOSIS AND TX
Distortion of shape of erythrocytes       Hemolytic Disease of Newborn (Erythroblastosis Fetalis)	Premature rupture of RBC -        Genetics -        Toxins, parasites   Rh Incompatibility  mother’s antibody attack RBC of fetus lyses

Types of anemia: HYDROPS FETALIS

DESCRIPTION	CAUSE	S/X	DIAGNOSIS AND TX
Abnormal fluid accumulation in fetal compartment  swelling or edema	Immune cause: Rh incompatibility Non-immune: genetic, infections (CMV and parvovirus)

Types of anemia: THALASSEMIA

DESCRIPTION	CAUSE	S/X	DIAGNOSIS AND TX
Abnormal hemoglobin production Microcytic, hypochromic and short lived   B Thalassemia -        Minor -        Major A Thalassemia -        Secret carrier -        Minor -        HbH disease -        Hydrops Fetalis	Mutation in genes       Beta chain defect -        Only one defective -        Both are defective Alpha chain defect -        One gene -        Two gene -        Three genes -        All 4 genes

Types of anemia: APLASTIC ANEMIA

DESCRIPTION	CAUSE	S/X	DIAGNOSIS AND TX
Decrease in production of all types of blood cells in bone marrow   Pancytopenia – reduction in all 3 major blood cells (when px has aplastic anemia, pancytopenia is also usually observed)	Toxins (damage bone marrow) Radiation therapy, chemo		Bone marrow transplant w/ immunosuppression

Types of anemia: SICKLE CELL ANEMIA

DESCRIPTION	CAUSE	S/X	DIAGNOSIS AND TX
Abnormal HgB in RBC  sickle shape cells that rupture easily and obstruct BV	Hemolytic anemia (low oxygen) Inherited (SCA genes) -        If heterozygous = protected against malaria -        If homozygous = more susceptible	Hand-foot syndrome (in children)  swelling of feet and wrists Pain in limbs and back (elderly)	Analgesic, antibiotic, blood transfusion

Types of anemia: POLYCYTHEMIA

DESCRIPTION	CAUSE	S/X	DIAGNOSIS AND TX
Over 65% RBC -        Inc viscousity, BP -        Thrombosis (smaller bv)	Abnormal increase in circulating RBC count		Hematocrit test

Leukemia

DESCRIPTION	CAUSE	S/X	DIAGNOSIS AND TX
Abnormal increase in WBC   Acute = immature leukocytes a.     Acute lymphoblastic b.     Acute myeloid Chronic = mature leukocytes a.     Chronic lymphocytic b.     Chronic myeloid	Origin location: myelocytic, lymphocytic and monocytic   Lymphoid, children, rapid progression Myeloid, child and adult, rapid   Lymphocytes, adult, slow Myeloid, adults

Diagnosis for infectious mononucleosis

DESCRIPTION	CAUSE	S/X	DIAGNOSIS AND TX
Abnormal increase in WBC   Acute = immature leukocytes a.     Acute lymphoblastic b.     Acute myeloid Chronic = mature leukocytes a.     Chronic lymphocytic b.     Chronic myeloid	Origin location: myelocytic, lymphocytic and monocytic   Lymphoid, children, rapid progression Myeloid, child and adult, rapid   Lymphocytes, adult, slow Myeloid, adults

Blood

-        only liquid ct

-        vs. water: more heavy, thick and viscous. Only 8% of body weight

Component of Blood:

1.     Plasma – protein albumin, electrolytes and gases (O2 + CO2)

2.     Erythrocytes – rbc

3.     Buffy coat

Component of plasma

1.     Water (91.5%)

2.     Solutes (8.5%)

a.     Proteins – Albumin, Fibrinogen (for clotting)

b.     Electrolytes

c.     Enzymes

d.     Wastes – uric acid etc

Layers of Digestive system

1. mucosa

2. submucosa

3. muscular layer

4. serosa

5. enteric nervous systemEpithelium

Epithelium

1. Non-keratinized stratified squamous epithelium – mouth, pharynx, esophagus, anal canal

2. Simple columnar epithelium – stomach and intestines (secretion, absorption)

Lamina propia

areolar CT + lymphatic, blood vessels

• main route of absorption

• Contains mucosa-associated lymphoid tissue (MALT)

Muscularis mucosae

Layer of smooth muscle fibers

Creates many folds – increased surface area

Mucosa

1. Epithelium

2. Lamina propia

3. Muscularis mucosae

Submucosa

more areolar CT, more lymphatic and blood vessels

Muscular layer

1. skeletal muscle — Mouth, pharynx, superior/middle esophagus, external anal sphincter; The things you need to exert effort for

2. smooth muscle — Inner layer of circular fibers + outer layer of sheets; involuntary contractions

serosa / visceral peritoneum

Areolar CT + simple squamous epithelium

Enteric nervous system

branching network of motor neurons, interneurons, sensory neurons

At the cellular level, there are the myenteric and submucosal plexuses

1. Myenteric neural plexus – between circular & longitudinal smooth muscle

   Motor neurons: GI motility (frequency, strength of contraction)

2. Submucosal neural plexus – secretory cells of submucosa

   Motor neurons: Control secretions

Teeth structure: Gums, periodontium, dentin, dental alveolus, pulp cavity, root canal, dentinal tubule, periodontal ligament, apical foramen

1. Gums/gingivae – cover alveolar processes

2. Periodontium – all structures attaching tooth to dental alveolus of mandible/maxillary’s alveolar process

3. Dentin – found deeper to the enamel; makes up most of the teeth; calcified connective tissue (majority of tooth) protected by:

   1. Enamel – (Ca₃(PO₄)₂ + CaCO₃) (phosphates & carbonates). Made of calcium salt which protects the teeth from wear and tear.

4. Dental Alveolus – together with the gums, involved in periodontics

5. Pulp cavity – space enclosed by dentin; contains dental pulp (connective tissue containing nerves and blood vessels.)

6. Root canal – extension of pulp cavity that contains nerves and Bvs; for a root canal procedure to be successful, all tissues should be removed (to prevent bacterial growth)

7. Dentinal tubule – contains processes of odontoblasts and fluid.

8. Periodontal ligament – help anchor tooth to the underlying bone

9. Apical Foramen – an opening at the base of the root canal through which blood vessels, lymphatic vessels, and nerves enter a tooth.

Lip structure: Hard palate, soft palate, uvula, cheek, molars, premolars, canines, incisors, oral vestibule, labial frenulum, gingiva, fauces, tongue, lingual frenulum

1. Hard palate – bony; forms most of the roof of the mouth.

2. Soft palate – muscular; forms the rest of the mouth’s roof.

3. Uvula – prevent swallowed food from entering the nasal cavity

4. Cheek – forms lateral wall of oral cavity

5. Molars – grind food

6. Premolars – crush and grind food

7. Canines – tear food

8. Incisors – cut food

9. Oral vestibule – space between the cheeks and lips, and the gums and teeth.

10. Labial frenulum (Superior and Inferior) – attaches superior or inferior lip to gum.

11. Gingiva – gums

12. Fauces – opening between the oral cavity and oropharynx

13. Tongue – lifted upward; forms the floor of the mouth, manipulates food for chewing and swallowing, shapes food and senses taste.

14. Lingual frenulum – limits movement of the tongue posteriorly

Aphthous Stomatitis

Aphthous Stomatitis (canker sores or singaw)

Cause: Multifactorial. Drugs, stress, trauma, micronutrient deficiencies, oral hygiene, etc. Pharmacologic treatment: no official treatment Non-pharmacologic treatment: whatever works for your body (e.g. less pain)

Dental Caries

Dental Caries (tooth decay)

Factors (4): bacteria biofilm carbohydrates/sugar – need for fermentation into acidic components because hydroxyapatite becomes soluble in acidic environments  carbonic acid – found in sodas oral hygiene Mediated by dental biofilm + Dietary fermentable carbs + Oral hygiene problems + low Fluoride → brittle bone recommendation: do not wash the toothpaste off with water, just spit out the saliva and toothpaste mixture)

Solutes in saliva

• Ions (Na⁺, K⁺, Cl^-, HCO₃^- & PO₄^3-) – amylase activator (Cl^-), buffer (HCO₃^-, PO₄^3- + urea + proteins)

• Gases

• Urea, uric acid – waste removal

• Mucus (more in sublingual > submandibular – for lubrication)

• IgA – prevents microbe attachment to epithelium

• Enzymes: lysozyme, salivary amylase (parotid)

Sialorrhea

Sialorrhea

Excess salivation Main receptor: muscarinic (M1 and M3) receptors for parasympathetic stimulation Sympathetic Nervous System can have its effects in hypersalivation/sialorrhea through adrenergic receptors, which are next to the blood vessels of salivary glands. More sympathetic activation → more adrenaline → vasoconstriction → squeeze more saliva out of the salivary glands

Xerostomia

Xerostomia

Dry mouth Can be caused by autoimmune disease Sympathetic stimulation: Alpha-2 agonists → less NE release in the salivary gland → no vasoconstriction → no saliva secretion → dry mouth

Mucus

• Contains mucin (glycosylated/complex of proteins + enzymes + electrolytes) in viscoelastic 3D network

mucoadhesion

material (usually polymeric) adheres to mucus via interfacial forces of attraction

Two stages of mucoadhesion: contact and consolidation

Theories related to mucus

• Wetting — Adhesion is instigated by material penetration into the surface irregularities of mucus. Material hardening then occurs yielding adhesive connections. This theory is applicable to mucoadhesive materials of low viscosity.

• Electrostatic — At the interface between mucus and mucoadhesive material, electron transfer occurs, resulting in an electrical double layer at the interface with attractive forces maintaining adhesion.

• Diffusion — Mucoadhesive polymeric chains interact with glycoprotein mucin chains, and as a result of penetration (diffusion), leads to the formation of a semi-permanent bond which maintains adhesion.

• Absorption — After the contact stage of mucoadhesion, adhesion is due to surface forces on the materials in question (hydrophobic bonding, hydrogen bonding and van der Waal’s forces)

• Fracture — This theory can be thought of as the amount of force that is required to separate two adhered surfaces. This theory provides the rationale for the in vitro analysis of mucoadhesive strength with a texture analyser.

Digestion

1. Mechanical Digestion

• Chewing/mastication – tongue manipulation & teeth grinding + saliva

• Bolus formation

2. Chemical Digestion

• Salivary amylase – starches, disaccharides → monosaccharides

• Lingual lipase (acidic pH): TG → fatty acid + diglyceride

Pharynx

• Nasopharynx (respiratory)

• Oropharynx (respiratory + digestive)

• Laryngopharynx (respiratory + digestive)

Swallowing/deglutition

• Voluntary phase – tongue moves upwards, backward to push bolus

• Involuntary phase

  • Bolus stimulates oropharynx receptors

  • Impulses travel to deglutition center (medulla, brainstem lower pons)

  • Impulses go back → soft palate, uvula move up to close nasopharynx, epiglottis closes larynx

• Esophageal phase – peristalsis (series of contractions and relaxations)

Aspiration pneumonia

•  aspiration of oropharyngeal/gastric contents

  • Hypersalivation

  • Sedation

  • Paralysis of throat muscles

Esophagus

• Contains mucous cells near stomach

  • Muscle tissue:

    • Upper 1/3 = skeletal

      • Intermediate = skeletal/smooth

      • Lower 1/3 = smooth

    • Sphincters

      • Upper esophageal sphincter – pharynx to esophagus

      • Lower esophageal sphincter/LES (near heart) – esophagus to stomach

      • Gastroesophageal reflux disease/GERD – causes heartburn

stomach

• J-shaped digestive canal enlargement (most distensible)

• Functions

  • Mixing chamber

  • Holding reservoir

• Histology (vs rest of GI tract)

  • Simple columnar epithelium: surface mucous cells

  • Epithelial cells extending to lamina propria: gastric glands

Mucous neck cells

mucus + HCO₃^- (release and repair stimulated by prostaglandins)

Parietal cells

• secrete HCl (Stomach acid; H⁺ and Cl^-) — Due to this, those who vomit a lot may suffer damages in the esophagus upwards due to the acid, as well as hypochloridia (a deficiency in Cl^-).  

Intrinsic factor

helps with the absorption and transport of cyanocobalamin

H⁺ (via H+/K+ ATPase), Cl^-

• Denatures proteins; inactivates salivary amylase; activates lingual lipase

• H⁺ from H₂CO₃ formed by carbonic anhydrase

• Omeprazole blocks H⁺/K⁺ ATPase > less proton secretion.  

• Chief/zymogenic cells

• Pepsinogen – +HCl → pepsin (peptidase)

  • Activated by acids

  • -gen — indicates that it is a precursor to an enzyme.

  • protein enzymes are often stored in inactive form is because otherwise, all the proteins in the body would be metabolized

• Gastric lipase – TGs → FAs + monoglycerides

G cell

gastrin: stimulate HCl secretion

Peptic Ulcer Disease

Peptic Ulcer Disease

Causative Agent: Helicobacter pylori (causes 70-80% of ulcers, majority), NSAIDs (2nd most common cause) NOT all ulcers are caused by H. pylori. If caused by H. pylori: treatment is usually a combination of around 4 medicines (2 antibiotics, 1 proton pump inhibitor, and 1 antacid (bismuth))  Gastric ulcer – stomach Duodenal ulcer – intestines Sx: excruciating pain, as well as “urea breath”. Balance between aggressive (acid, pepsin) and protective (mucosal defense, repair) factors. Epidemiologic data DOES NOT support an association for coffee and ulcers.

Gastroesophageal Reflux Disease (GERD)

Gastroesophageal Reflux Disease (GERD)

Reflux of stomach contents causes extraesophageal effects, such as tooth decay, dental erosion, and sore throat, as well as cardiac and pulmonary complications. Sx: Heartburn, regurgitation, belching, etc. GERD ≠ hyperacidity ≠ increase in acid. GERD is defined as a reflux disease. Less of an acid, more of a reflux. Pathophysiology Gastric Factors — same H+ secretion but w/ “acid pocket”, delayed gastric emptying In GERD, the acid pockets are NOT affected by the acid buffering effect of food in addition to delayed gastric emptying, hence, the acids tend to go up. Anti-reflux barrier — LES (lower esophageal sphincter) relaxations (may happen when you swallow, eat, sleep, or even for unknown reasons), low LES pressure Chyme — when the mixture of digested food and acid reaches the intestines. Refluxate — when mixture of digested food and acid goes in the opposite direction. Refluxate – acid reflux (pH<4) & bile reflux (↑permeability, heartburn, PPI resistance), gas reflux (belching), weakly acidic reflux Bile — made of cholesterol and lecithin, which worsen the damage in the esophagus as they can help promote the penetration/permeability of the refluxate due to its more lipophilic nature; originally helpful in the absorption in the intestine through the emulsification of the fatty components. No Acid ≠ No bile. Thus, even without acid reflux, it is possible to have bile reflux.  Gas reflux may also occur. This makes the refluxate remain acidic, even after taking antacids (omeprazole).  Proximal extent & esophageal distention Esophageal clearance Peristalsis (initial (smooth muscle contraction) & secondary/ distention-induced) Chemical clearance – saliva swallowing; can wash off refluxate from the esophagus. Normal people (those without GERD) may have reflux from time to time, except they have efficient clearance mechanisms Last line; if refluxate still is NOT yet cleared, this may lead to esophagitis (inflammation of the esophagus).  Esophagitis — Refluxate enters mucosal breaks → activates sensory afferent nerves & stimulates release of pro-inflammatory cytokines, promoting pain, damage, and inflammation.  Epithelial cell proliferation change, attraction of T-lymphocytes & other inflammatory cells

Why can GERD be triggered when someone lies down?

Anatomic. Depending on direction–for instance, if you have a weak sphincter and you lean to the left, the stomach contents are pushed towards the esophageal sphincter. On the other hand, if you lean to the right, the stomach contents are pushed towards the pyloric sphincter. This is one factor for increased gastric emptying.

Panceatic enzymes

• Carbohydrate digestion: Pancreatic amylase

• Protein digestion: Trypsin, Chymotrypsin, Carboxypeptidase, Elastase

  • Secreted in inactive form: trypsinogen, chymotrypsinogen, procarboxypeptidase, proelastase

  • Trypsinogen – (enterokinase) → Trypsin → activates other 3 precursors

• Triglyceride digestion: Pancreatic lipase

Nucleic acid digestion: Ribonuclease and deoxyribonuclease

Why is pancreatin taken while standing up for px with pancreas problems?

if taken while sitting or lying down, the capsule will bump into the esophagus or stomach, causing it to release its components early and act on/digest those parts which may cause pain.

Hepatic sinusoids

• Permeable blood capillaries between hepatocytes

  • Receive O₂’d blood from hepatic artery branches & nutrient-rich de-O2’d blood from hepatic portal vein branches

  • Contain stellate reticuloendothelial cells / hepatic macrophages / Kupffer cells

Cholesterol gallstones

• Cholesterol hypersecretion – insulin resistance, estrogen, cholesterol transporters

• Supersaturated bile, rapid phase transition – pro-nucleating factors (e.g. mucins from saliva)

• Gallbladder hypomotility (smooth muscles not moving, increasing the chances for bile to solidify) – stiffened smooth muscle cells from cholesteryl esters & inflammation

• Intestinal factors – bile diverted to intestines due to hypomotility metabolized by bacteria into deoxycholate → more hepatic cholesterol secretion, crystallization

Brown pigment gallstones

• abnormal bilirubin metabolism

  • Black – Ca²⁺ bilirubinate or polymers (Ca²⁺ + Cu²⁺ + unconjugated bilirubin + Ca²⁺ bilirubinate)

  • Brown – Ca²⁺ salts of unconjugated bilirubin + misc (cholesterol, FAs, mucin, bile salts, phospholipids, bacterial residue – esp E. coli)

Fatty Liver Disease

Fatty Liver Disease

Phased out: “alcoholic” vs “non-alcoholic”, “fatty” liver disease  New umbrella: Steatotic Liver Disease (SLD) Main causes: fat (triglycerol) accumulation in liver or Hepatic steatosis (TAG accumulation in liver) detected via imaging/biopsy More fat → lipid storage increases → increases scarring → liver goes haywire (liver dysfunction) Activating the thyroid hormone can speed up the metabolism in the liver, help clear excess fat due to their calorigenic effect (heat generating property) and becomes a reason why heat generation and weight loss as usual symptoms of excess thyroid hormones/ hyperthyroidism

Advanced Liver Injury: Cirrhosis

Advanced Liver Injury: Cirrhosis

Also called hepatitis Definition: liver tissue scarring Other causes: HBV, HCV, alcohol, metabolic,autoimmune, biliary, vascular, drug-induced Triglycerol accumulate → Inflammation → Hepatic stellate cells (vit. A storage) activated → vit A loss → fibrotic scar tissue synthesis / scarring → cirrhosis Can lead to portal hypertension →  complications: Ascites — peritoneal cavity fluid accumulation. brought by activation of RAAS → increased sodium-water retention → increase blood hydrostatic pressure → leaking, causing ascites VS edema: vary on location edema: peripheral ascites: peritoneal cavity Variceal bleeding  Acute kidney injury–hepatorenal syndrome Hepatic encephalopathy – NH3, etc. Caused by amino acid deamination from glutamine to glutamate → release NH3 (ammonia) → NH3 goes to the brain, resulting to hepatic encephalopathy Bacterial infections Portal vein thrombosis

Epithelial cells of small intestine

• Absorptive cells – enzymes, microvilli

• Goblet cells – mucus

• Paneth cells – lysozymes

• Enteroendocrine cells – S, L, K, & CCK cells