GI Digest Nzym Parasite Dfens Mech MCQ's

Explanation
Glycerol is least likely to be expected in an analysis of a mixed micelle because it is a polar molecule and does not readily associate with nonpolar molecules like fatty acids, cholesterol, lysophospholipids, and monoglycerides. Mixed micelles are formed by the aggregation of nonpolar molecules in the presence of bile salts, and glycerol, being polar, would not be able to effectively incorporate into these micelles. Therefore, it is the least likely product of lipid digestion to be found in a mixed micelle analysis.

Explanation
The sucrase-isomaltase complex is responsible for the cleavage of a-limit dextrin. This complex is produced by the enterocytes in the brush border of the small intestine. Sucrase breaks down sucrose into glucose and fructose, while isomaltase breaks down isomaltose and a-limit dextrin into glucose. Therefore, the sucrase-isomaltase complex plays a crucial role in the digestion of carbohydrates in the small intestine.

Explanation
NADH dehydrogenase (also referred to as NADH:ubiquinone reductase or Complex I) is an enzyme located in the inner mitochondrial membrane that catalyzes the transfer of electrons from NADH to coenzyme Q (CoQ). It is the "entry enzyme" of oxidative phosphorylation in the mitochondria
NADH Dehydrogenase is the first enzyme (Complex I) of the mitochondrial electron transport chain. There are three energy-transducing enzymes in the electron transport chain - NADH dehydrogenase (Complex I), Coenzyme Q – cytochrome c reductase (Complex III), and cytochrome c oxidase (Complex IV). NADH dehydrogenase is the largest and most complicated enzyme of the electron transport chain.
The reaction of NADH dehydrogenase is:
NADH + (H+) + CoQ + 4(H+)in → NAD+ + CoQH2 + 4(H+)out
In this process, the complex translocates four protons across the inner membrane per molecule of oxidized NADH, helping to build the electrochemical potential used to produce ATP.
The reaction can be reversed - referred to as aerobic succinate-supported NAD+ reduction - in the presence of a high membrane potential, but the exact catalytic mechanism remains unknown
(MOA) All redox reactions take place in the extramembranous portion of NADH dehydrogenase. NADH initially binds to NADH dehydrogenase, and transfers two electrons to the flavin mononucleotide (FMN) prosthetic group of complex I, creating FMNH2. The electron acceptor - the isoalloxazine ring - of FMN is identical to that of FAD. The electrons are then transferred through the second prosthetic group of NADH dehydrogenase via a series of iron-sulfur (Fe-S) clusters, and finally to coenzyme Q (ubiquinone). This electron flow changes the redox state of the protein, inducing conformational changes of the protein which alters the pK values of ionizable side chain, and causes four hydrogen ions to be pumped out of the mitochondrial matrix. Ubiquinone (CoQ) accepts two electrons to be reduced to ubiquionol (CoQH2).
The best-known inhibitor of Complex I is rotenone (commonly used as an organic pesticide). Rotenone and rotenoids are isoflavonoids occurring in several genera of tropical plants such as Antonia (Loganiaceae), Derris and Lonchocarpus (Faboideae, Fabaceae). There have been reports of Indians using rotenone-containing plants to fish - due to its ichthyotoxic effect - as early as the 17th century. Rotenone binds to the ubiquinone binding site of Complex I as well as piericidin A, another potent inhibitor with a close structural homologue to ubiquinone.
Mutations in the subunits of Complex I can cause mitochondrial diseases, including Leigh syndrome. Point mutations in various Complex I subunits derived from mitochondrial DNA (mtDNA) can also result in Leber's Hereditary Optic Neuropathy. There is some evidence that Complex I defects may play a role in the etiology of Parkinson's disease, perhaps because of reactive oxygen species (Complex I can, like Complex III, leak electrons to oxygen, forming highly toxic superoxide).

Explanation
Metabolic dysfunctions in mitochondria can lead to a decrease in energy production, resulting in fatigue. Metabolic acidosis occurs when there is an accumulation of acid in the body due to impaired metabolism. This can cause symptoms such as fatigue, weakness, and confusion. Therefore, the clinical symptoms associated with metabolic dysfunctions in mitochondria are fatigue and metabolic acidosis.

Explanation
The given symptoms of severe acidosis, vomiting, hypotonia, and neurologic deficits, along with elevated levels of lactate and alanine in the serum, suggest a deficiency in Pyruvate dehydrogenase. Pyruvate dehydrogenase is an enzyme involved in the conversion of pyruvate to acetyl-CoA, which is an important step in the production of energy in the form of ATP. A deficiency in this enzyme leads to the accumulation of pyruvate and lactate, causing the symptoms observed in the newborn.

Explanation
(short answer) Fructose is by facilitated difusion, Gluc/gala use Na co-transport

Mechanisms of transport:
Monosaccharides must next be transported across the luminal membrane of the enterocyte. The sodium/glucose transporter 1 (SGLT1) is a symporter that takes up glucose (and galactose) against its concentration gradient by coupling its transport to that of Na+. Once inside the cytosol, glucose and galactose can be retained for the epithelium's metabolic needs or can exit the cell across its basolateral membrane via facilitated diffusion by a transporter known as GLUT2. Movement of sodium and glucose is an important driving force for water absorption, because accumulation of these solutes on the serosal side provides an efficient driving force for osmotic water absorption.

Fructose, in contrast, is taken up across the apical membrane by via GLUT5. Fructose may exit the cell through GLUT5, but the main pathway is via GLUT2.

A key point to understand is that because fructose transport is not coupled to that of Na+, its uptake in comparison is relatively inefficient, and the transporters become saturated if large quantities of food containing free fructose are ingested and fructose is not absorbed – this causes osmotic retention of water in the lumen. The symptoms that occur from this malabsorption are similar to those experienced by a lactose-intolerant patient who consumes lactose. (slide 18 small-intst&colon-White)

Explanation
Amylase is the correct answer because it is a pancreatic enzyme that is secreted into the duodenum and has its primary action in the duodenum. Amylase breaks down starches and carbohydrates into smaller molecules such as glucose, which can then be absorbed by the small intestine. This enzyme is active in the optimal pH range of 6.8 - 8.0, which is achieved in the small intestine.

Explanation
Thiamin deficiency in alcoholics decreases the activity of a-ketoglutarate dehydrogenase, which is an enzyme involved in the TCA cycle. This leads to a slower TCA cycle. Additionally, this deficiency also decreases the activity of pyruvate dehydrogenase, another mitochondrial enzyme. As a result, pyruvate accumulates and lactic acidosis occurs. Therefore, the correct answer is Pyruvate dehydrogenase.

Explanation
according to buxbaum we should know that in this part of France they use Riccotta CHEESE to prepare their spinach. He also says 2hrs is too soon for food poisoning. (has he ever eaten at the shacks?)

Explanation
The most likely diagnosis for this patient is Familial hypercholesterolemia (FH). This is supported by the high levels of cholesterol, LDL, and triglycerides in the lab investigations. Additionally, the presence of nodules on the hands, elbows, and Achilles tendons is consistent with xanthomas, which are commonly seen in patients with FH. The family history of early myocardial infarction also suggests a genetic component, further supporting the diagnosis of FH. Diabetes mellitus type I, MODY, metabolic syndrome, and neurofibromatosis are not consistent with the patient's presentation and lab results.

Explanation
A patient with a genetic defect causing lower activity of disaccharidases would have difficulty breaking down disaccharides such as maltose, sucrose, and lactose into their monosaccharide components. As a result, these undigested disaccharides would pass through the digestive system and be excreted in the stool. Therefore, the patient would exhibit higher levels of maltose, sucrose, and lactose in the stool compared to a normal person.

Explanation
The presence of hydrochloric acid is the most responsible factor for the elimination of microorganisms in the human stomach. Hydrochloric acid creates an acidic environment in the stomach, which is inhospitable for many microorganisms. The low pH of the stomach acid helps to kill or inhibit the growth of bacteria, viruses, and other pathogens that may be ingested with food or water. This acidic environment is an important defense mechanism of the body to prevent infections and maintain a healthy digestive system.

Explanation
Plasmodium spp. (blood & tissue) TISSUE SPOROZOA
Vertebrates: intermediate hosts
Mosquito: definitive host
(slide 30-33-Protozology-Adebiyi)

Explanation
Paneth cells are specialized epithelial cells found in the small intestine. They are known for their antimicrobial activity and secretion of various proteins, such as defensins and lysozyme, which help in the defense against pathogens. Neutrophils, similarly, are a type of white blood cells that are also involved in the immune response against infections. They are known for their ability to phagocytose and kill pathogens. Therefore, Paneth cells most resemble neutrophils in terms of their biological activity, as both are involved in the defense against pathogens.

Explanation
Trichinella spiralis is a nematode parasite, occurring in rats, pigs, bears and humans, and is responsible for the disease trichinosis. It is sometimes referred to as the "pork worm" due to it being found commonly in undercooked pork products.
Trichinella species are the smallest nematode parasite of humans, have an unusual life cycle and are one of the most widespread and clinically important parasites in the world.[1] The small adult worms mature in the intestines of an intermediate host such as a pig. Each adult female produces batches of live larvae, which bore through the intestinal wall, enter the blood (to feed on it) and lymphatic system, and are carried to striated muscle Once in the muscle, they encyst, or become enclosed in a capsule. Humans can be infected by eating infected pork or wild carnivores such as fox, cat or bear.[
Trichinella spiralis is a parasitic nematode that has a direct life cycle, meaning it completes all stages of development in one host. The larval forms are encapsulated as a small cystic structure within the infected host. Humans typically become infected when they eat improperly cooked pork or Trichinella infected meat. When a human eats the infected meat, the larvae are released from the nurse cell (due to stomach pH) and migrate to the intestine, where they burrow into the intestinal mucosa, mature, and reproduce.[2] It is interesting to note that juveniles within nurse cells have an anaerobic or facultative anaerobic metabolism, but when they become activated, they adopt an aerobic metabolism characteristics of the adult. Female Trichinella worms live for about six weeks, and in that time can produce up to 1,500 larvae; when a spent female dies, she passes out of the host. The larvae can then gain access to the circulation and migrate around the body of the host. The migration and encystment of larvae can cause fever and pain brought upon by the host inflammatory response. In some cases, migration to specific organ tissues can cause myocarditis and encephalitis that can result in death.

Explanation
Cutaneous leishmaniasis (also known as "Leishmaniasis tropica,") is the most common form of leishmaniasis. It is a skin infection caused by a single-celled parasite that is transmitted by SANDFLY bites. There are about 20 species of Leishmania that may cause cutaneous leishmaniasis.
Diagnosis
Diagnosis is based on the characteristic appearance of non-healing raised, scaling lesions that may ulcerate and become secondarily infected with organisms such as Staphylococcus aureus, in someone who has returned from an endemic area. The gold standard for diagnosis is PCR.

Pathophysiology
Promastigotes of leishmania are transmitted to human skin by the bite of a sandfly. Leishmania then invades human macrophages and replicates intracellularly.
A raised, red lesion develops at the site of the bite (often weeks or sometimes years afterwards). The lesion then ulcerates and may become secondarily infected with bacteria. In many species (for example, L. major) the lesion often spontaneously heals with atrophic scarring. In some species (for example, L. viannia braziliensis) the lesion may spontaneously heal with scarring, but then re-appear elsewhere (especially as destructive mucocutaneous lesions). Lesions of other leishmania species may spontaneously heal and then re-appear as satellite lesions around the site of the original lesion, or along the route of lymphatic drainage.
Some species tend to cause cutaneous leishmaniasis (e.g., L. major and L.tropica), whereas some species tend to cause visceral leishmaniasis (e.g., L. infantum and L donovani), though emerging research (due to high deployment rates of western countries to indigenous areas) is showing these species specific presentation lines are blurring

Explanation
Onchocerciasis also known as river blindness and Robles' disease, is a parasitic disease caused by infection by Onchocerca volvulus, a nematode (roundworm).
Onchocerciasis is the world's second-leading infectious cause of blindness. It is not the nematode, but its endosymbiont, Wolbachia pipientis, that causes the severe inflammatory response that leaves many blind. The parasite is transmitted to humans through the bite of a black fly of the genus Simulium. The larval nematodes spread throughout the body. When the worms die, their Wolbachia symbionts are released, triggering a host immune system response that can cause severe itching, and can destroy optical tissue in the eye.
The vast majority of infections occur in sub-Saharan Africa, although cases have also been reported in Yemen and isolated areas of Central and South America. An estimated 18 million people suffer from onchocerciasis, with approximately 270,000 cases of blindness related to the infection.
Signs and symptoms
Adult worms remain in subcutaneous nodules, limiting access to the host's immune system.[ Microfilariae, in contrast, are able to induce intense inflammatory responses, especially upon their death. Dying microfilariae have been recently discovered to release Wolbachia surface protein that activates TLR2 and TLR4, triggering innate immune responses and producing the inflammation and its associated morbidity.[9] Wolbachia species have been found to be endosymbionts of O. volvulus adults and microfilariae, and are thought to be the driving force behind most of O. volvulus morbidity. The severity of illness is directly proportional to the number of infected microfilariae and the power of the resultant inflammatory response
Skin involvement typically consists of intense itching, swelling, and inflammation. A grading system has been developed to categorize the degree of skin involvement
• Acute papular onchodermatitis - scattered pruritic papules,
• Chronic papular onchodermatitis - larger papules, resulting in hyperpigmentation,
• Lichenified onchodermatitis - hyperpigmented papules and plaques, with edema, Lymphadenopathy, pruritus and common secondary bacterial infections,
• Skin atrophy - loss of elasticity, the skin resembles tissue paper, 'lizard skin' appearance, and
• Depigmentation - 'leopard skin' appearance, usually on anterior lower leg.
Ocular involvement provides the common name associated with onchocerciasis, river blindness, and may involve any part of the eye from conjunctiva and cornea to uvea and posterior segment, including the retina and optic nerve.[ The microfilariae migrate to the surface of the cornea. Punctate keratitis occurs in the infected area. This clears up as the inflammation subsides. However, if the infection is chronic, sclerosing keratitis can occur, making the affected area become opaque. Over time, the entire cornea may become opaque, thus leading to blindness. Some evidence suggests the effect on the cornea is caused by an immune response to bacteria present in the worms..As the skin is itchy, it can lead to severe rashes and you can permanently kill off patches of skin.

Explanation
The women and children who tend the mulberry bushes and use human feces for manure are at the highest risk for hookworm infection. Hookworms are parasites that commonly infect humans through contaminated soil. The practice of stomping down the feces with bare feet increases the likelihood of coming into contact with the hookworm larvae, which can penetrate the skin and cause infection. Ascariasis, trichinosis, and trichuris infection are not directly related to the use of human feces as manure and are therefore less likely to be the correct answer in this context.

Explanation
Onchocerciasis also known as river blindness and Robles' disease, is a parasitic disease caused by infection by Onchocerca volvulus, a nematode (roundworm).
Onchocerciasis is the world's second-leading infectious cause of blindness. It is not the nematode, but its endosymbiont, Wolbachia pipientis, that causes the severe inflammatory response that leaves many blind. The parasite is transmitted to humans through the bite of a black fly of the genus Simulium. The larval nematodes spread throughout the body. When the worms die, their Wolbachia symbionts are released, triggering a host immune system response that can cause severe itching, and can destroy optical tissue in the eye.
The vast majority of infections occur in sub-Saharan Africa, although cases have also been reported in Yemen and isolated areas of Central and South America. An estimated 18 million people suffer from onchocerciasis, with approximately 270,000 cases of blindness related to the infection.
Signs and symptoms
Adult worms remain in subcutaneous nodules, limiting access to the host's immune system.[ Microfilariae, in contrast, are able to induce intense inflammatory responses, especially upon their death. Dying microfilariae have been recently discovered to release Wolbachia surface protein that activates TLR2 and TLR4, triggering innate immune responses and producing the inflammation and its associated morbidity.[9] Wolbachia species have been found to be endosymbionts of O. volvulus adults and microfilariae, and are thought to be the driving force behind most of O. volvulus morbidity. The severity of illness is directly proportional to the number of infected microfilariae and the power of the resultant inflammatory response
Skin involvement typically consists of intense itching, swelling, and inflammation. A grading system has been developed to categorize the degree of skin involvement
• Acute papular onchodermatitis - scattered pruritic papules,
• Chronic papular onchodermatitis - larger papules, resulting in hyperpigmentation,
• Lichenified onchodermatitis - hyperpigmented papules and plaques, with edema, Lymphadenopathy, pruritus and common secondary bacterial infections,
• Skin atrophy - loss of elasticity, the skin resembles tissue paper, 'lizard skin' appearance, and
• Depigmentation - 'leopard skin' appearance, usually on anterior lower leg.
Ocular involvement provides the common name associated with onchocerciasis, river blindness, and may involve any part of the eye from conjunctiva and cornea to uvea and posterior segment, including the retina and optic nerve.[ The microfilariae migrate to the surface of the cornea. Punctate keratitis occurs in the infected area. This clears up as the inflammation subsides. However, if the infection is chronic, sclerosing keratitis can occur, making the affected area become opaque. Over time, the entire cornea may become opaque, thus leading to blindness. Some evidence suggests the effect on the cornea is caused by an immune response to bacteria present in the worms..As the skin is itchy, it can lead to severe rashes and you can permanently kill off patches of skin.

Explanation
(tsetste rhymes w/ gambiese)

The insect vector for T. brucei is the TSETSE fly. The parasite lives in the midgut of the fly (procyclic form), whereupon it migrates to the salivary glands for injection to the mammalian host on biting. The parasite lives within the bloodstream (bloodstream form) where it can reinfect the fly vector after biting. Later during a T. brucei infection the parasite may migrate to other areas of the host. A T. brucei infection may be transferred human to human via bodily fluid exchange, primarily blood transfer.

Explanation
(think, vaginal=sperm=flagella)
Diagnosis Trichomonas vaginalis (UROGENITAL FLAGELLATE) : flagella appears “jerky”
Classically, with a cervical smear, infected women have a transparent "halo" around their superficial cell nucleus. It is unreliably detected by studying a genital discharge or with a cervical smear because of their low sensitivity. T. vaginalis was traditionally diagnosed via a wet mount, in which "corkscrew" motility was observed. Currently, the most common method of diagnosis is via overnight culture, with a sensitivity range of 75-95%

Explanation
Trichinella spiralis is a nematode parasite, occurring in rats, pigs, bears and humans, and is responsible for the disease trichinosis. It is sometimes referred to as the "pork worm" due to it being found commonly in undercooked pork products.
Trichinella species are the smallest nematode parasite of humans, have an unusual life cycle and are one of the most widespread and clinically important parasites in the world.[1] The small adult worms mature in the intestines of an intermediate host such as a pig. Each adult female produces batches of live larvae, which bore through the intestinal wall, enter the blood (to feed on it) and lymphatic system, and are carried to striated muscle Once in the muscle, they encyst, or become enclosed in a capsule. Humans can be infected by eating infected pork or wild carnivores such as fox, cat or bear.[
Trichinella spiralis is a parasitic nematode that has a direct life cycle, meaning it completes all stages of development in one host. The larval forms are encapsulated as a small cystic structure within the infected host. Humans typically become infected when they eat improperly cooked pork or Trichinella infected meat. When a human eats the infected meat, the larvae are released from the nurse cell (due to stomach pH) and migrate to the intestine, where they burrow into the intestinal mucosa, mature, and reproduce.[2] It is interesting to note that juveniles within nurse cells have an anaerobic or facultative anaerobic metabolism, but when they become activated, they adopt an aerobic metabolism characteristics of the adult.[1] Female Trichinella worms live for about six weeks, and in that time can produce up to 1,500 larvae; when a spent female dies, she passes out of the host. The larvae can then gain access to the circulation and migrate around the body of the host.[2] The migration and encystment of larvae can cause fever and pain brought upon by the host inflammatory response. In some cases, migration to specific organ tissues can cause myocarditis and encephalitis that can result in death.

Explanation
Taenia saginata, also known as Taeniarhynchus saginata or the beef tapeworm, is a parasite of both cattle and humans, causing taeniasis in humans. Taenia saginata occurs where cattle are raised by infected humans maintaining poor hygiene, human feces are improperly disposed of, meat inspection programs are poor, and where meat is eaten without proper cooking. The disease is relatively common in Africa, some parts of Eastern Europe, Southeast Asia, and Latin America.
Symptoms
Tapeworms are usually asymptomatic. However heavy infection often results in weight loss, dizziness, abdominal pain, diarrhea, headaches, nausea, constipation, or chronic indigestion, and loss of appetite. There can be intestinal obstruction in humans and this can be alleviated by surgery

The basic **DIAGNOSIS** is done from a stool sample. Feces are examined to find parasite eggs.
(ironically, even parasites can be infected with parasites)

Explanation
Cutaneous leishmaniasis (also known as "Leishmaniasis tropica,") is the most common form of leishmaniasis. It is a skin infection caused by a single-celled parasite that is transmitted by SANDFLY bites. There are about 20 species of Leishmania that may cause cutaneous leishmaniasis.
Diagnosis
Diagnosis is based on the characteristic appearance of non-healing raised, scaling lesions that may ulcerate and become secondarily infected with organisms such as Staphylococcus aureus, in someone who has returned from an endemic area. The gold standard for diagnosis is PCR.

Pathophysiology
Promastigotes of leishmania are transmitted to human skin by the bite of a sandfly. Leishmania then invades human macrophages and replicates intracellularly.
A raised, red lesion develops at the site of the bite (often weeks or sometimes years afterwards). The lesion then ulcerates and may become secondarily infected with bacteria. In many species (for example, L. major) the lesion often spontaneously heals with atrophic scarring. In some species (for example, L. viannia braziliensis) the lesion may spontaneously heal with scarring, but then re-appear elsewhere (especially as destructive mucocutaneous lesions). Lesions of other leishmania species may spontaneously heal and then re-appear as satellite lesions around the site of the original lesion, or along the route of lymphatic drainage.
Some species tend to cause cutaneous leishmaniasis (e.g., L. major and L.tropica), whereas some species tend to cause visceral leishmaniasis (e.g., L. infantum and L donovani), though emerging research (due to high deployment rates of western countries to indigenous areas) is showing these species specific presentation lines are blurring